1. family and parenting
2. children

Copyright 1999 by the American Psychological Association, Inc.
0033-295X/99/S3.00
Psychological Review
1999, Vol. 106, No. 3, 458-490
Risk for Psychopathology in the Children of Depressed Mothers:
A Developmental Model for Understanding Mechanisms of Transmission
Ian H. Gotlib
Sherryl H. Goodman
Stanford University
Emory University
A large body of literature documents the adverse effects of maternal depression on the functioning and
development of offspring. Although investigators have identified factors associated with risk for
abnormal development and psychopathology in the children, little attention has been paid to the
mechanisms explaining the transmission of risk from the mothers to the children. Moreover, no existing
model both guides understanding of the various processes' interrelatedness and considers the role of
development in explicating the manifestation of risk in the children. This article proposes a developmentally sensitive, integrative model for understanding children's risk in relation to maternal depression.
Four mechanisms through which risk might be transmitted are evaluated: (a) heritability of depression;
(b) innate dysfunctional neuroregulatory mechanisms; (c) exposure to negative maternal cognitions,
behaviors, and affect; and (d) the stressful context of the children's lives. Three factors that might
moderate this risk are considered: (a) the father's health and involvement with the child, (b) the course
and timing of the mother's depression, and (c) characteristics of the child. Relevant issues are discussed,
and promising directions for future research are suggested.
depressed mothers are at risk for abnormal development and have
begun to identify factors that are associated with this risk. Despite
this shift in focus, however, we currently have little understanding
of why and how these children are at risk. That is, relative to our
knowledge of the range of adverse outcomes for children of
depressed mothers, we know little about the mechanisms that
underlie the risk for these outcomes. What are the likely mechanisms through which risk for adverse outcomes in children of
depressed mothers might be transmitted? How might multiple
mechanisms interact when they co-occur? How are specific mechanisms related to particular outcomes in the children? In what
ways might mechanisms feed back to each other in bidirectional or
dynamic processes? What are the possible or likely pathways to
disorder in children of depressed mothers? And what is the role of
developmental factors in the association between depression in
mothers and the emergence of psychopathology in the children?
The purpose of this article is to propose and begin to evaluate an
integrative, developmentally sensitive model for the understanding
of children's risk as a function of maternal depression. The major
goals in presenting this model are to (a) address mechanisms
underlying the elevated risk for dysfunction that characterizes
children of depressed mothers, (b) cut across the lines that have
traditionally separated studies of genetic-biological factors and
investigations of cognitive-interpersonal factors in depression, and
Much has been written about the adverse effects of mothers'
depression on their children. Most of that work has focused on
documenting the negative outcomes in functioning and diagnostic
status of children whose mothers are clinically or subclinically depressed. Given the consistency of the results of studies in this area,
there is no question that children are adversely affected by their
mothers' depression.1 Indeed, negative effects of maternal depression
have been documented in children ranging in age from infancy
through adolescence. For example, compared with offspring of nondepressed controls, infants of depressed mothers have been found to
be more fussy, to obtain lower scores on measures of mental and
motor development, and to have more difficult temperaments and less
secure attachments to their mothers. Toddlers of depressed mothers
have been found to react more negatively to stress and to be delayed
in their acquisition of effective self-regulation strategies. Finally,
relative to control children, school-aged children and adolescents
whose mothers are depressed have been found to have more school
problems, to be less socially competent, and to have lower levels of
self-esteem and higher levels of behavior problems (for recent reviews
of these literatures see Cummings & Davies, 1994; Gotlib & Goodman, 1999; and Gotlib & Lee, 1996).
Recently, researchers have attempted to move beyond an examination of the relatively simple question of whether children of
Sherryl H. Goodman, Department of Psychology, Emory University; Ian
H. Gotlib, Department of Psychology, Stanford University.
Preparation of this article was supported by Grant MH 59259 from the
National Institute of Mental Health.
We thank Donna Gelfand and Mahzarin Banaji for their helpful comments on a draft of this article.
Correspondence concerning this article should be addressed to Sherryl
H. Goodman, Department of Psychology, 532 Kilgo Circle, Emory
University, Atlanta, Georgia 30322. Electronic mail may be sent to
[email protected].
'Although fathers may also pose a risk for their children, the focus of
this article is on depression in mothers. Women experience clinically
significant depression at about twice the rate as men (Blehar & Oren,
1995). In part because of this gender difference, women have been the
focus of the vast majority of the scientific studies in the area of depressive
disorders. Moreover, as we contend later in this article, because of their
role women are implicated specifically in several of the risk mechanisms
proposed in this article.
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RISK FOR PSYCHOPATHOLOGY
(c) be consistent with principles of developmental psychopathology. Although the functioning of children of depressed mothers
has been the subject of a number of reviews (e.g., Cummings &
Davies, 1994; Field, 1992; Gelfand & Teti, 1990; Goodman, 1992;
Gotlib & Goodman, 1999; Gotlib & Lee, 1990, 1996; Hammen,
1991), the present article is unique in proposing and evaluating an
integrative, developmentally sensitive theoretical model of the
mechanisms of risk. Unlike those earlier reviews, the present
article is not a comprehensive review of the descriptive literature
examining the functioning of offspring of depressed mothers.
Rather, the primary goals of this article are to propose and evaluate
an integrative model of risk to children of depressed mothers and
to set an agenda to guide future process research in this area.
We begin by introducing three principles that guided our development of the conceptual model: the role of a model, the need to
consider reciprocal and transactional relationships, and the need to
take a developmental perspective. Then we present the model,
briefly discussing its components and outlining possible patterns
of dynamic interplay among the components. Next, we discuss
four mechanisms through which we propose that risk to the children of depressed mothers might be conferred: (a) heritability of
depression; (b) innate dysfunctional neuroregulatory mechanisms;
(c) exposure to negative maternal cognitions, behaviors, and affect; and (d) the stressful context of the children's lives. For each
of the mechanisms, we review the results of relevant studies and
summarize the status of current knowledge. We then present a
similar review of three potential moderators of the association
between maternal depression and negative outcomes in the children: the father's health and involvement with the child, the course
and timing of the mother's depression, and characteristics of the
child, such as gender and temperament.
In the final section of the article, we raise several issues, and, in
the context of those issues, we identify both theoretical and empirical gaps in our knowledge and provide what we believe are
promising directions for future research in this field. First, we
consider the strengths and limitations of the proposed mechanisms,
focusing on the extent to which each mechanism has been supported by the empirical literature. We also examine the extent to
which each mechanism addresses and accounts for reciprocal and
transactional relationships between parent and child and among
risk factors, and we examine whether it suggests developmental
pathways to disorder in the children of depressed mothers. Second,
we consider the level of theory that is most needed, arguing
strongly for the advantages of an integrative model such as the one
proposed in this article. Third, we examine the specificity of the
model and the findings to maternal depression and to depression as
the outcome of risk in the children. In this context we discuss the
potential role of specific correlates of maternal depression and the
difficulties engendered when investigators do not consider these
correlates in their studies. Fourth, we explore the notions of
sensitive periods and children's recovery from adversity.
Principles Guiding the Development of the
Conceptual Model
The Role of a Model
Essentially, a model of risk in this area must provide guides to
identifying variables that mediate or moderate the association
459
between parental depression and negative outcome in the children
(Baron & Kenny, 1986). Mediation refers to mechanisms through
which maternal depression may be associated with adverse child
outcomes. Thus, factors that mediate may be any of the ways in
which children or families with a depressed mother (or the subset
of such children or families in which there are negative child
outcomes) differ from children or families without a depressed
mother (e.g., abnormal neuroregulatory mechanisms in the child,
high levels of family stress, parents' marital conflict, etc.). In
contrast, moderators refer to variables for which the effects of
maternal depression on child functioning are different at different
levels of that variable. Moderators, even those as simple as children's gender and age, might improve the predictive efficacy and
add important explanatory power concerning when, and under
what circumstances, maternal depression will be more strongly
associated with negative outcomes in the children. In general,
therefore, we must have a better understanding of both exacerbating and protective factors that contribute to the variability in the
outcomes of children of depressed mothers.
Reciprocal and Transactional Relationships
Investigators increasingly have recognized the importance of
both reciprocal and transactional relationships within families
(e.g., Bell & Harper, 1977; Sameroff, 1990). The child's characteristics may strongly influence his or her own developmental
course as a function of the complex interplay between the parents
and child over time (see, for instance, Lytton, 1990, on the contributions to antisocial behavior). For example, both gender and
temperament are likely to play significant roles in the development
of patterns of family interaction and in the emergence of psychopathology. Moreover, although we do not yet fully understand the
natural course of disorders in childhood, it is likely that the
emergence of risk factors at various points in the child's trajectory
influence and change that trajectory, just as the current status of a
child or family system may influence the emergence of a risk
factor (cf. Gotlib & Wheaton, 1997). Finally, it is also important to
consider reciprocal and transactional relations among the factors
that both mediate and moderate the association between maternal
depression and child outcome and how they may influence the
developmental trajectory toward disorder. We discuss this position
more fully later in this article.
A Developmental Perspective
In general, a developmental perspective has been lacking in
studies of children of depressed mothers. Knowledge of underlying
developmental processes is critical to the study of risk for the
development of psychopathology in children, as well as to the
understanding of failures in the development of competence (Cicchetti & Schneider-Rosen, 1986). Moreover, a solid understanding
of developmental processes is also crucial in designing preventive
interventions for children at risk for psychopathology (Goodman,
1984). To date, researchers have tended to study children of
depressed mothers either in one developmental period or in such a
broad age range that two or more distinct developmental stages are
included (and confounded). Both these strategies fail to address
developmental issues. Conclusions drawn from studies of children
in one developmental stage cannot be presumed to generalize to
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GOODMAN AND GOTLIB
another period in children's lives. Moreover, studies that group
together children whose ages vary widely likely mask important
developmental issues.
From a developmental perspective, it is also essential to consider the timing of the mother's depressive episode, especially of
the first depressive episode during the child's lifetime, with respect
to the age of the child. A developmental theory of risk must be
sensitive to the normative maturational tasks that the child is
attempting to master at the time of exposure to the mother's
depression. In general, the older the child at the age of first
exposure, the more likely it is that behavioral systems will have
matured and, thus, that the child will be less vulnerable to adverse
influences. It is also more likely that the child will have developed
competencies that prepare him or her for successful coping (Compas, 1987; Sroufe & Rutter, 1984).
A related issue involves the fact that, unlike other stressors to
which children may be exposed, depression in adults is typically
not a single, time-limited event. In fact, as many as 25% of major
depressions may be chronic (Depue & Monroe, 1986). Moreover,
depression is also a recurrent disorder: Over 80% of depressed
patients have more than one depressive episode (Belsher &
Costello, 1988). More than 50% relapse within 2 years of recovery
(e.g., Keller & Shapiro, 1981; Mueller et al., 1996); indeed, individuals with three or more previous episodes of depression may
have a relapse rate as high as 40% within only 12 to 15 weeks after
recovery (Keller, Shapiro, Lavori, & Wolfe, 1982; Keller et al.,
1992). Clearly, therefore, few children are exposed to only one
episode of maternal depression. Unfortunately, researchers rarely
assess and report either the child's age at first exposure or the
number of episodes to which the child has been exposed (see
Goodman, Brogan, Lynch, & Fielding, 1993, and Hammen, Burge,
& Adrian, 1991, for exceptions). Because of this limitation, we are
not able to draw on empirical data to evaluate this important
developmental consideration. We do, however, provide some suggestions for research that would address these concerns.
Finally, a hallmark of the developmental psychopathology perspective is an examination of the pathways to disorder, including
the causes and consequences of the emergence of risk factors in the
children. The adverse outcomes that have been identified in children of depressed mothers, such as depression and other emotional
disorders and adjustment difficulties, are known to unfold over
time. Characteristics or tendencies of the children's behavior,
affect, or psychobiological functioning may be risk factors or early
signs of a disorder that has not yet emerged. These same characteristics and tendencies, therefore, may contribute to the increased
risk for the disorder. In addition, some children will develop signs
of maladjustment that may or may not progress to disorder. We
evaluate our proposed model for its potential to address these
issues of alternative pathways to disorder.
An Integrative Model of the Transmission of Risk to
Children of Depressed Mothers
A model that will significantly advance the study of children of
depressed mothers is one that integrates biological and environmental considerations within a transactional perspective, that acknowledges the crucial role played by factors that may mediate
and moderate the effects of maternal depression on children, and
that is sensitive to developmental issues. Such an integrative model
is presented in Figure 1. Essentially, as can be seen from Figure 1,
the model posits that there are four potential mechanisms through
which maternal depression adversely affects child functioning. In
addition, we propose three factors that may moderate the association between maternal depression and child dysfunction.
The first point in this model is a depressed mother.2 In turn,
having a depressed mother increases the likelihood of the presence
and operation of one or more of four proposed mechanisms for the
transmission of risk to the child: (a) heritability of depression; (b)
innate dysfunctional neuroregulatory mechanisms; (c) negative
maternal cognitions, behaviors, and affect; and (d) the stressful
context of the children's lives. Although all of these represent
potential mechanisms for the transmission of risk for psychopathology, any particular depressed mother-child dyad may be characterized by one, more than one, or, arguably least frequently,
none of these mechanisms.
The model assumes further that a number of the proposed
mechanisms will interact with one another and, consequently, is
intended as a guide for exploring such interactions as they may
affect the transmission of risk. In particular, genetic factors probably interact with all of the other mechanisms and moderators.
Similarly, biological and psychosocial mechanisms also likely
interact. Later in this article we describe the potential benefits of
exploring gene-environment interactions, correlations, and covariation, and we describe stress-diathesis models.
As indicated in Figure 1, the occurrence of one or more of the
proposed mechanisms for the transmission of risk is associated
with the emergence of vulnerabilities in the offspring in any of
several domains of functioning, including psychobiological (the
central nervous system, especially the hypothalamic-pituitaryadrenocortical [HPA] axis), cognitive (e.g., dysfunctional cognitions, low self-esteem, helplessness or hopelessness beliefs, biased
attention or memory functioning), affective (e.g., low stress resilience, difficulties in emotional regulation), and behavioral or interpersonal (e.g., inadequate social and social-cognitive skills,
dysfunctional impulse control, problems in concentration, low
mastery motivation).
Although we have presented these vulnerabilities as discrete
categories, it is important to recognize that they, like the risk
mechanisms, will almost certainly interact and affect one another.
For example, children who are characterized by dysregulation of
the HPA axis may be predisposed both to act in a lethargic manner
and to exhibit hyper-responsiveness to the challenges of novel
environments (Coplan et al., 1996). These tendencies would be
expected to lead to a low rate of rewarding experiences, another
vulnerability to depression. Furthermore, as part of a dynamic
family system in which these behaviors in the child are exhibited
to the mother, they may lead to an increase in maternal stress,
lower maternal perceived parenting efficacy, and poorer quality of
mother-child interactions. In essence, therefore, this proposed
model for the transmission of risk to children of depressed mothers
2
It should be pointed out here that a number of factors, both alone and
in interaction, affect the probability of depression in a mother (e.g., genetic
factors, cognitive vulnerability, stressful life events, etc.). It is beyond the
scope of this article to review these disparate literatures, but specific
studies and findings are presented and integrated in this article when they
are relevant.
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RISK FOR PSYCHOPATHOLOGY
Mechanisms
[
I
• Psychobiological dysfunction
• Skills deficits or maladaptive
styles or behavioral tendencies
• Cognitive
• Affective
• Behavioral or interpersonal
Heritability of
depression
Depressed
Mother
Innate
dysfunctional
neuroregulatory
mechanisms
Moderators
• Fathers
• Availability
• Mental health
• Timing and course of
Mother's depression
• Characteristics of the child
• Temperament
• Gender
• Intellectual and
social-cognitive skills
Figure 1.
Exposure to
mother's
negative and/or
maladaptive
cognitions,
behaviors,
and affect
Vulnerabilities
• Childhood or
adolescent
depression
• Other
disorders
,
Exposure
to stressful
environment
An integrative model for the transmission of risk to children of depressed mothers.
reflects the reality of bio-behavioral organisms, in that biological
aspects of functioning are inextricably linked with psychological
aspects of functioning. That link has been absent from most of the
research on children with depressed mothers.
Finally, the model proposes that these vulnerabilities interact
with three potential moderators: the father's health and involvement with the child, the course and timing of the mother's depression, and characteristics of the child, such as gender and temperament. The interactions of these vulnerabilities and moderators
increase the likelihood of the development of psychopathology in
childhood or adolescence, or, at a minimum, deficits in social,
emotional, or cognitive functioning. We turn now to an extended
discussion of each of the four proposed mechanisms for the transmission of risk to children of depressed mothers.
Mechanisms of Transmission of Risk
What is it about having a depressed mother that places a child at
increased risk for abnormal development? As we noted above, we
propose four possible mechanisms for the transmission of risk to
children of depressed mothers, as well as three variables that might
moderate these associations. Two of the proposed mechanisms are
primarily biological in nature: One focuses on genetic factors (the
heritability either of depression per se or of vulnerabilities to
depression), and the other implicates dysfunctions in innate neu-
roregulation. The third mechanism focuses on disturbed interpersonal processes between depressed mothers and their children
including children's exposure to and social learning of their mothers' maladaptive or negative cognitions, behavior, and affect.
Finally, the fourth mechanism for the transmission of risk implicates the stressful context of the children's lives.
Mechanism 1: Having a Depressed Mother Confers on
the Child a Genetic Predisposition to Depression
Mechanism 1 explains in simple terms that children born to
mothers who are, or who have been, depressed inherit DNA that is
different in important ways from that inherited by children of
nondepressed mothers. The DNA is assumed to regulate the biological mechanisms of these children in ways that serve to increase
or decrease their vulnerability to depression. Thus, children of
depressed mothers may inherit directly a vulnerability to
depression.
It is also possible that, in the same manner, children of depressed mothers inherit vulnerabilities to personality traits, cognitive or interpersonal style variables, or environmental characteristics or experiences, which themselves increase the risk for the
development of depression. Examples of such variables include
inhibited temperamental style, shyness, negative affectivity, low
self-esteem, negatively biased perceptions of the environment, low
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GOODMAN AND GOTLIB
sociability, and the likelihood of experiencing poor parenting
quality, life stress, and parental marital conflict and divorce. These
variables could increase the risk for depression in children by
leading them to select or avoid particular types of environments, to
attend or respond selectively to certain aspects of their environments, thereby resulting in biased perceptions of the interpersonal
world, or to experience a disproportionate number of stressors.
These characteristics, in turn, may place the child at increased risk
for developing a depressive disorder. In this section of the article,
we examine evidence for both direct and indirect heritability of
vulnerability to depression.
Empirical support. There is a considerable body of literature
demonstrating a consistent pattern of genetic transmission of depressive disorders in adults. Considering all of the data obtained in
investigations using twin, adoption, and family study designs, the
risk for an affective disorder in adult first-degree relatives of a
patient with unipolar affective disorder is estimated at 20-25%,
compared with a general population risk of 7% (for reviews see
Nurnberger, Goldin, & Gershon, 1986; Tsuang & Faraone, 1990).
In addition to this high heritability of adult depression, two
specific findings are particularly relevant for the study of children
with depressed mothers, one concerning the severity of the mother's depression and the other involving the timing of the mother's
depression. The first finding concerns the issue of clinical versus
subclinical levels of depression. The relevant finding from recent
twin studies is that narrowly defined major (i.e., clinically significant) depression is associated with high heritability (i.e., 79% of
the variance accounted for by additive genetic effects) and only a
small role of a common family environment; in contrast, the more
common, milder (i.e., subclinical) forms of depression in adults
appear to be influenced predominantly by environmental factors
(e.g., Kendler et al., 1995; Kendler, Neale, Kessler, Heath, &
Eaves, 1993; McGuffin & Katz, 1993; McGuffin et al., 1993;
Plomin, 1990). Thus, studies examining women who are clinically
depressed may differ from investigations focusing on women who
are characterized by elevated scores on depression rating scales in
the extent to which pathology in the child is mediated genetically.
The second finding from the genetic investigations of adult
depression that is relevant to the study of children of depressed
mothers involves the timing of the mother's depression with respect to the age of the child. Weissman et al. (1984) found that
adult depressives with onset before age 20 have a higher familial
aggregation than do those with later onsets. Moreover, compared
with women with lower familial aggregation, women with higher
familial aggregation have been found to be more likely to experience postpartum depression in response to the normal challenges
of pregnancy and childbirth (O'Hara, 1986).3 The implications of
these findings for genetic risk to children are important but are
rarely acknowledged: Offspring of mothers with early-onset depression, particularly during the postpartum period, may carry a
higher heritability for depression than do children whose mothers'
depressions occur later in their lives (cf. Weissman, Warner,
Wickramaratne, & Prusoff, 1988).
In sum, there is little question that depression in adults has a
high degree of heritability. It is important, however, to examine
more directly the heritability of depression occurring in childhood,
particularly given the high rates of depression that have been
documented in children of depressed mothers. Although studies of
family history, or family aggregation, offer some support for the
heritability of childhood-onset depression, they have an inherent
limitation of not being able to disentangle influences of genetic
factors and family environment (but see Todd, Neuman, Geller,
Fox, & Hickok, 1993, for an application of segregation analysis to
address this limitation). Merikangas, Weissman, Prusoff, and John
(1988) found that the presence of a depressed spouse or of firstdegree relatives with a psychiatric illness increased the risk of a
psychiatric diagnosis in the children of depressed mothers. Similarly, Weissman et al. (1987) reported that children who become
depressed manifest the disorder at an earlier age (M age of onset = 12.7 years) if they have a depressed mother than if their
mother is not depressed (M age of onset = 16.8 years). Moreover,
Weissman et al. (1988) found that early-onset depression in a
mother (i.e., before age 20) was associated with a 14-fold increase
in the risk of onset of major depression before age 13 years in their
children. Weissman et al. interpreted this finding as further evidence for greater genetic contribution to depression in the offspring of parents with early-onset major depression. It seems clear,
therefore, that depression in parents and other first-degree relatives
increases the risk for depression in children and adolescents.
Other family studies in which a depressed child, rather than a
depressed adult or parent, is identified as the proband have reported elevated prevalence rates for affective disorders among
first- and second-degree adult relatives. This pattern has been
obtained with relatives of depressed prepubertal children (aged
6-12 years; Kovacs, Devlin, Pollock, Richards, & Mukerji, 1997;
Puig-Antich et al., 1989; Todd, Geller, Neuman, Fox, & Hickok,
1996; Todd et al., 1993), of depressed adolescents (mean age 15
years; Kutcher & Marlon, 1991; Williamson et al., 1995), and of a
mixed-age group of 7- to 17-year-old depressed children (Mitchell,
McCauley, Burke, Calderon, & Schloredt, 1989). Moreover, the
results of segregation analyses conducted by Todd et al. (1993)
indicate not only that genetic transmission of risk is more important than environmental transmission but, further, that transmission
appears to conform to an additive model of risk; that is, the degree
of risk increases in a linear fashion with the number of affected
relatives. Considered collectively, the results of these studies highlight the importance of genetic transmission of risk in child- and
adolescent-onset depression.
Consistent with importance of early-onset depression described
above, other investigators have found rates of depressive illness to
be higher in relatives of depressed children than they are in
relatives of both depressed adolescents (e.g., Williamson et al.,
1995) and depressed adults (Kovacs et al., 1997). Interestingly,
both Williamson et al. and Kovacs et al. found that first-degree
relatives of depressed children or adolescents with comorbid behavior disorders (e.g., attention deficit disorder, conduct disorder,
and substance use-abuse disorders) themselves had higher rates of
alcoholism, substance abuse, and antisocial personality disorders.
These findings are discussed later in this article with respect to the
issues of the specificity of children's risk to maternal depression,
3
Earlier age of onset of depression in women would increase the
likelihood both that their children would be exposed early in their development and, given the high rates of recurrence of depression, that they
would be exposed to multiple episodes. Thus, early exposure to maternal
depression is likely confounded with higher genetic risk. We expand on
this point later in the article.
RISK FOR PSYCHOPATHOLOGY
rather than its correlates (including comorbid disorders) and with
respect to the need to explicate alternative models to explain
different outcomes for children of depressed mothers.
Four recent twin studies provide more direct tests of this proposed genetic mechanism of transmission of risk. Those studies
demonstrate that the extent of genetic influence varies considerably with the child's severity of depression, the age of onset of
depression, and the child's gender. Importantly, however, all of
those studies are limited by having examined the genetic contribution to risk for depressive symptoms rather than for diagnosed
depression.
With respect to severity of the child's depression, Rende, Plomin, Reiss, and Hetherington (1993) conducted a twin and halfsibling study analysis of 9- to 18-year-olds using scores on the
Children's Depression Inventory (GDI; Kovacs, 1992). Rende et
al. found moderate support for heritability of depressive symptoms
(the individual heritability estimate, h2, was significant at .34 ±
.14) and little support for shared environmental influence. Interestingly, however, when the same analyses were conducted for the
subgroup of children who scored above a clinical cutoff on the
GDI, the results were reversed: Genetic influence was no longer
significant, but shared environmental influences were significant.
Harrington, Rutter, and Fombonne (1996) and Thapar and
McGuffin (1996) found that in 8- to 10-year-old twins, depressive
symptoms, measured by summing parents' and children's scores
on a shortened Mood and Feelings Questionnaire (MFQ; Costello
& Angold, 1988), were more strongly associated with family
discord and other qualities of shared environmental factors than
they were with genetic factors. In contrast, in older (11- to 16year-old) twins, depressive symptoms were more strongly associated with genetic than with environmental factors. Consistent with
this pattern of results, K. T. Murray and Sines (1996) found that for
4- to 6-year-old twins, variance in the mothers' scores on the
Missouri Children's Behavior Checklist (MCBL) was explained
by environmental factors only (predominantly nonshared environmental factors). In contrast, for older (7- to 12-year-old) twins,
nearly half of the variance in mothers' MCBL scores was attributable to genetic factors, with nonshared environmental factors
accounting for the remainder.
Finally, with respect to gender, K. T. Murray and Sines (1996)
also found different loadings of genetic and environmental factors
for boys and girls in explaining transmission of depressive symptoms. For girls, additive genetic factors accounted for about 40%
of the variance in mothers' MCBL scores, and both shared and
nonshared family environmental factors contributed significantly
to the equation. In contrast, for boys only nonshared environmental
factors accounted for significant proportions of the variance in the
MCBL scores. Thus, there is no single estimate of the extent of
genetic contribution to children's depressive symptoms, with the
estimate varying by severity of symptoms and children's age and
gender.
We now turn to the question of heritability of specific traits or
environmental factors that increase vulnerability to depression.
Behavior genetics analyses have demonstrated that several correlates of, if not risk factors for, depression in children are highly
heritable (for a review, see Loehlin, 1992). These factors include
temperament (H. H. Goldsmith, Buss, & Lemery, 1997; Plomin et
al., 1993), behavioral inhibition and shyness (Cherny, Fulker,
Corley, Plomin, & DeFries, 1994), low self-esteem (Loehlin &
463
Nichols, 1976), neuroticism (Tellegen et al., 1988), sociability
(Plomin et al., 1993), subjective well-being (Lykken & Tellegen,
1996), and expression of negative emotion (Plomin et al., 1993).
Although not yet examined in children, genetic factors have also
been found to contribute to individual differences in perceived
adequacy of social support and the availability of a close and
confiding relationship but not in the quantity or frequency of social
interactions (cf. Bergeman, Plomin, Pedersen, McClearn, & Nesselroade, 1990; Kessler, Kendler, Heath, Neale, & Eaves, 1992;
Roberts & Gotlib, 1997). Importantly, both Bergman et al. and
Kessler et al. found support for partial genetic mediation of the
well-established association between social support and risk for
depression (cf. Cohen & Wills, 1985).
A number of theorists have recently contended that many of the
environmental variables that increase children's vulnerability to
depression may themselves be heritable. For example, Plomin
(1994) argued that genetic factors contribute to differences in
variables such as poor parenting quality, life stress, and marital
conflict, which have typically been conceptualized as "environmental" rather than as genetically mediated. Indeed, using quantitative genetic methods and analyses, researchers have now demonstrated that genetic factors contribute to both self-reported and
observed parenting and family environment measures (Braungart,
1994; O'Connor, Hetherington, Reiss, & Plomin, 1995; Plomin,
Reiss, Hetherington, & Howe, 1994). In these studies, adopted
monozygotic twins were found to be more similar to each other
than were adopted dizygotic twins with respect to several aspects
of their family environments, even though both types of twins had
been reared apart. In fact, almost 25% of the variance in family
environment was found to be genetic in origin (O'Connor et al.,
1995; Plomin et al., 1994). Similarly, Kendler, Neale, Heath,
Kessler, and Eaves (1991), McGuffin and Katz (1993), and Plomin
(1990) all recently reported evidence indicating that life events or
stressors, which often have been associated with depression (cf.
Brown & Harris, 1978), have a significant genetic component. And
McGue and Lykken (1992) found strong evidence for the influence
of genetic factors in the risk for divorce. Thus, the likelihood that
children will experience stressful environments also appears to be
genetically mediated.
Summary. The strongest and clearest conclusion that can be
drawn from the genetics research reviewed above is that there is a
substantial genetic contribution to depression in adults. The genetic contribution in adults appears to be greater for depression
that meets diagnostic criteria than for depression that is measured
solely by scores on symptom checklists; the genetic contribution is
also greater for early- than for late-onset depressions. Given that
the major outcome of interest among children with depressed
mothers is depression occurring during childhood or adolescence,
however, we also examined evidence that genetic vulnerability
mediates these early-onset depressions. The support for heritability
of childhood- or adolescence-onset depression is less clear than
that for adult-onset depression. The strongest support comes from
familial aggregation studies, although they are characterized by a
number of inherent limitations. Findings from the twin studies are
inconclusive and, further, are limited to children's depressive
symptoms rather than clinically significant depression.
At this point, therefore, we cannot make strong statements
concerning the extent to which heritability mediates the association between maternal depression and child psychopathology. In
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GOODMAN AND GOTLIB
addition, the strength of the genetic contribution appears to vary
with a number of factors. For example, for less severe childhood
depression, and for girls, heritability has been found to be a
stronger factor than are environmental variables. In contrast, for
more severe levels of depression in children and particularly in
boys, environmental factors seem to have a stronger influence than
does heritability. Finally, the genetic model also contributes to our
understanding of the issue of specificity of outcome for the children of depressed mothers. That is, familial patterns of transmission from parent to child seem to include the common comorbid
disorders of alcoholism, substance abuse, and conduct-antisocial
personality disorders, suggesting that the risk to children of depressed mothers is nonspecific, with respect to both the risk factors
for psychopathology in the children and the diverse outcomes that
the children experience.
Finally, the studies that are relevant to the possibility of inherited vulnerabilities to depression contribute to our understanding
of children of depressed mothers in several respects. First, they
correct inaccurate but prevalent conceptualizations of environmental variables that result from not taking into consideration their
substantial genetic influences. Second, these studies broaden the
perspective taken by more traditional genetic positions by suggesting that children of depressed mothers might inherit not only a
tendency to experience depression but also an elevated risk of
acquiring personal characteristics that are associated with vulnerability to depression and an elevated risk of experiencing stressful
life events, including exposure to poor parenting, marital conflict,
and their parents' divorce. All of these personal tendencies and
experiences could be triggers for later depressive episodes in
individuals who are already sensitized or vulnerable to depression.
Third, and perhaps most importantly, these studies provide an
opportunity to reconsider our assumptions about the mechanisms
by which such variables as parenting, life stress, and divorce might
influence children of depressed mothers. At minimum, psychosocial models alone, such as parental role models or models focusing
on poor parenting, are inadequate to explain the association between maternal depression and child dysfunction. Nevertheless,
despite the strong evidence for heritability of many of the risk
factors for depression, studies have not yet been conducted explicitly to test the role of heritability of these risk factors as mediators
of the association between maternal depression and psychopathology in the children.
Mechanism 2: Infants of Depressed Mothers Are Born
With Dysfunctional Neuroregulatory Mechanisms That
Interfere With Emotional Regulation Processes and,
Consequently, Increase Vulnerability to Depression4
Mechanism 2 proposes that children of depressed mothers are
born with dysfunctional neuroregulatory mechanisms. Although
these may be a function of either genetic factors or adverse
prenatal experiences, in this section we place a greater emphasis on
the latter possibility. That is, the dysfunctional neuroregulatory
mechanisms are hypothesized to be a direct effect of abnormal
fetal developments caused by the mothers' depression during
pregnancy; these abnormal developments could be due to such
factors as the fetus' exposure to the neuroendocrine alterations
associated with the mother's depression, constricted blood flow to
the fetus, and so on. Thus, this mechanism is restricted to infants
born to mothers who experience a clinically significant episode of
depression during the pregnancy or who suffered a previous episode from which their neuroendocrine dysfunction has not recovered. The proposed abnormal fetal developments may be manifested at birth as behavioral traits or tendencies, such as a tendency
to react to certain events with a particular response style (Calkins,
1994; Kagan, Reznick, & Snidman 1988). Examples might be
behavioral inhibition or negative affectivity. These traits or tendencies, in turn, increase children's vulnerability to develop depression. An alternative, diathesis-stress position is that the potential dysfunction is actualized or manifested only in the context of
a particular social environmental history (Kagan, 1994).
Empirical support. Support for Mechanism 2 comes primarily
from two sets of studies. The first set of investigations includes
studies examining the fetal environment provided by depressed
women. Researchers in this area have focused on how particular
aspects of the fetal environment may lead to abnormal fetal developments, which manifest themselves at birth as dysfunctional
neuroregulatory mechanisms. In a second set of studies, researchers have examined newborns of depressed mothers for behavioral
evidence of dysfunctional neuroregulatory mechanisms, with the
assumption that these dysfunctions are related to adverse in utero
environments.
Among the first set of studies, researchers have examined aspects of the fetal environment that may be specific to depressed
women and that may be associated with abnormal fetal development. Among the factors that have been considered as possible
mechanisms of abnormal fetal development among depressed
women are (a) neuroendocrine abnormalities, (b) reduced blood
flow to the fetus, (c) poor health behaviors, and (d) the use of
antidepressant medication.
With respect to the neuroendocrine abnormalities, an important
question to be addressed is whether the neuroendocrine correlates
of the mother's depression are experienced by the fetus via utero
blood flow. Because development begins in utero and the fetus'
first transaction with the mother occurs at gestational days 13-14,
when utero blood flow is established, the fetus might be affected
by the neuroendocrine correlates of the mother's depression well
before birth. Two studies examined the neurobiology of pregnant,
depressed women and found plasma cortisol, beta-endorphin, and
corticotrophin releasing hormone (CRH) levels to be higher among
women who rated elevated levels of depressed mood at 28 to 38
weeks of gestation (Handley, Dunn, Waldron, & Baker, 1980;
Smith et al., 1990). Similarly, Field (1998) found higher urinary
cortisol and norepinephrine in depressed pregnant women. Studies
of stress during pregnancy, which is generally highly correlated
with depression (e.g., Hammen, 1990; Lewinsohn, Hoberman, &
Rosenbaum, 1988), similarly conclude that stress during pregnancy is associated with increased levels of catecholamines, epinephrine, and norepinephrine; acute stress may be associated with
cortisol release and immunosuppression (Emory, Hatch, Blackmore, & Strock, 1993). Thus, as a group depressed women are
4
Because these dysfunctions may reflect genetic risk, we could have
included them in the previous section. However, the dysfunctions may also
reflect in utero environmental hazards. Consequently, we are treating this
as a separate mechanism.
RISK FOR PSYCHOPATHOLOGY
characterized by abnormal neuroendocrine functioning during
pregnancy.
Few studies have examined specifically whether these hormones
cross the placenta to the fetus. Glover, Teixeira, Gitau, and Fisk
(1998) reported no significant correlation between fetal and maternal hormone levels at 20-36 weeks of pregnancy with the single
exception of cortisol; maternal levels of cortisol accounted for
50% of the variance in the fetus' levels of cortisol. This finding
suggests that maternal cortisol crosses the placenta. Our knowledge of the psychobiology of depression justifies our concern for
infants who, as fetuses, were exposed to corticotropin-releasing
factor (CRF) hypersecretion. The consequences for infants of such
exposure would be expected to be manifested in abnormal stress
reactivity, abnormal behavioral and affective functioning, and abnormal EEG patterns. Each of these aspects of functioning is
known to be disrupted in adult depression (Davidson & Fox, 1988;
Gotlib, Ranganath, & Rosenfeld, 1998; see Gotlib & Hammen,
1992, for a review of this research) and may represent markers of
risk for depression in the infants of depressed mothers (Field,
Pickens, Fox, Nawrocki, & Gonzalez, 1995).
The second factor that has been considered as a possible mechanism of abnormal fetal development among depressed women is
reduced blood flow to the fetus. Three studies are relevant to this
issue. Glover (1997) conducted ultrasound tests on 100 nonsmoking, healthy women in their third trimester of pregnancy and found
maternal trait anxiety to be associated with impaired uterine blood
flow. Glover also found that low uterine blood flow was also
associated with lower birth weight of the babies. Given the high
comorbidity of depression and anxiety, it is likely that this pattern
of findings would apply to depressed women as well. Interestingly,
in support of this contention, Field (1998) reported that fetuses of
women who were depressed during the pregnancy had lower
estimated weight and engaged in less movement (Field, 1998) than
did fetuses of control women. Finally, Emory, Walker, and Cruz
(1983) found that stress during pregnancy (itself a correlate of
depression) was associated with increased fetal heart rate, which in
turn, in uncomplicated pregnancies and deliveries, is associated
with lower attention orientation and arousal in the neonate. Considered together, these three studies provide indirect evidence that
maternal depression during pregnancy may be associated with
abnormal uterine blood flow and other difficulties in the fetuses
and neonates.
The third factor through which fetuses of depressed women may
be at elevated risk involves the inadequate health care and health
risk behaviors that have been found to be associated with depression. Milberger, Biederman, Faraone, Chen, and Jones (1996), for
example, found that depressed women are more likely than their
nondepressed counterparts to obtain and receive inadequate prenatal care, to report unhealthy eating and sleeping patterns, and to
engage in smoking. Each of these behaviors represents a risk factor
for abnormal development of the fetus (cf. Milberger et al., 1996).
Finally, several recent studies have addressed the question of
whether in utero exposure to antidepressant medications might
contribute to the development of abnormal neurophysiology in the
fetus. Both tricyclic antidepressants and fluoxetine, the two dominant medication treatments for major depression, do cross the
placental barrier. Interestingly, however, recent evidence suggests
that antidepressant medication taken during pregnancy has no
discernible adverse effects on the fetus or infant. Both Pastuszak et
465
al. (1993) and Chambers, Johnson, Dick, Felix, and Jones (1996)
found that tricyclic or fluoxetine exposure in the first trimester of
pregnancy was not related to increased risk of major malformations. And although Chambers et al. (1996) found increased risk
for perinatal complications in infants of women who took fluoxetine in their third trimester, they did not correct for the greater
severity of depression among women who needed continued medication throughout the pregnancy. More recently, Nulman et al.
(1997) examined 16-month-olds to 7-year-old children whose
mothers had received tricyclic antidepressants, fluoxetine, or no
antidepressant medication during pregnancy. Nulman et al. assessed the offsprings' neurocognitive development (the Bay ley
Scales of Infant Development or the McCarthy Scales of Children's Abilities), temperament, behavior problems, and language
skills and found no differences among the children of these three
groups of mothers on any of these measures.
In the second set of studies that are relevant to this proposed
mechanism for the transmission of risk to offspring of depressed
mothers, investigators have examined the status of neonates of
depressed mothers for behavioral evidence of dysfunctional neuroregulatory mechanisms. In one such set of studies, researchers
found increased rates of premature births and lower birth weight
among the neonates of depressed versus well mothers (e.g., Copper
et al., 1996; Hedegaard, Henriksen, Secher, Hatch, & Sabroe,
1996; Paarlberg, Vingerhoets, Passchier, Dekker, & Van Geijn,
1995). Field and her colleagues also hypothesized a prenatal origin
to the poor functioning of infants with depressed mothers (Field,
1992). They examined a group of mothers who had been identified
as depressed during a prenatal examination and were later diagnosed with postpartum depression. Within a few days after birth,
the neonates demonstrated poorer performance on the Brazelton
Neonatal Behavior Assessment Scale orientation and depression
clusters, including minimal responding to inanimate and social
stimuli (suggesting higher sensory thresholds), decreased motor
tone and lower activity levels, and less robustness and endurance
(Abrams, Field, Scafidi, & Prodromidis, 1995; Field, Sandberg,
Garcia, Vega-Lahr, Goldstein, & Guy, 1985). Finally, Zuckerman,
Bauchner, Parker, and Cabral (1990) studied a large group of
neonates at 8 to 72 hr after delivery and found a strong association
between mothers' depression symptom scores obtained during
pregnancy and excessive crying and inconsolability, as reported by
pediatricians who were blind to the mothers' depression scores.
These findings on the status of neonates are consistent with the
idea that infants of depressed mothers are born with dysfunctional
neuroregulatory mechanisms. However, they are only behavioral
manifestations and, as such, can only be suggested to reflect
neuroregulatory dysfunction. The young age at which the neonates
were studied makes it less likely that the measures reflect the
infant's early reaction to the depressed mother.
Some animal studies also have data relevant to the question of
innate dysfunctional neuroregulatory mechanisms. In studies of
rhesus monkeys, mild maternal stress during pregnancy (exposure
to unpredictable noise during mid-to-late gestation) was found to
be associated with offspring lower birth weight, poorer neuromotor
maturation, delayed cognitive development, and less exploration
of novel stimuli in infancy (Schneider, 1992). As juveniles, those
monkeys whose mothers had been stressed during pregnancy demonstrated abnormal social behavior and greater HPA activity (elevated cortisol) at baseline and, in particular, in response to stress
466
GOODMAN AND GOTLIB
(Clarke & Schneider, 1993; Clarke, Wittwer, Abbott, & Schneider,
1994). Similarly, rats that had been stressed by noise and light
during pregnancy had offspring with lower birth weight, less
vocalization during isolation in a novel environment, less exploration of novel environments, and suppressed immune function
(Kay, Tarcic, Poltyrev, & Weinstock, 1998; Poltyrev, Keshet, Kay,
& Weinstock, 1996; Williams, Hennessy, & Davis, 1998). Although not directly tested, the mechanism implicated in this set of
findings is an effect of maternal stress hormones on the developing
fetal neuroendocrine system.
Summary. Researchers are beginning to find that depressed
women have abnormal neuroendocrine functioning during pregnancy, that the fetus is exposed to an increase in cortisol level and
to less blood flow; perhaps as a consequence, the fetuses of
depressed women have also been found to be characterized by
relatively slow growth and less movement. Much of this research
is new and needs to be replicated. Other researchers have found
abnormalities in neonates born to women who had been depressed
during pregnancy. Although each of these early disturbances has
been hypothesized to contribute to the subsequent emergence of
psychopathology, none of these studies tested the role of these
early behavioral anomalies as mediators of the association between
maternal depression and depression in their children. For example,
premature birth and low birth weight have been identified as
increasing risk for mental retardation and for behavioral, emotional, and learning problems (Institute of Medicine, 1985; McGauhey, Starfield, Alexander, & Ensminger, 1991). These studies
are particularly important because they have assessed the infants'
functioning before the infants have been exposed behaviorally to
the depressed mother and therefore implicate abnormal fetal environments in the infants' abnormal functioning. Nonetheless, studies have not yet been conducted that would establish the roles of
these variables as mediators of the association between maternal
depression and psychopathology in the children.
Mechanism 3: Depressed Mothers Expose Their Children
to Negative or Maladaptive Cognitions, Behaviors, and
Affect, Which Places the Children at Elevated Risk
for Developing Depression
Mechanism 3 entails a number of related components. First,
depression in the parent is postulated to be associated with negative cognitions, behaviors, and affect. Second, because of these
depressive cognitions, behaviors, and affect, the depressed parent
is hypothesized to be an inadequate social partner for the child and
to be unable to meet the child's social and emotional needs. The
third component of this mechanism maintains that this inadequate
parenting would negatively affect the child's development of social and cognitive skills and styles. Fourth, we postulate that
through social learning or modeling, children acquire cognitions,
behaviors, and affect that resemble those exhibited by their depressed mothers. The fifth and final component of this mechanism
maintains that the children's acquired depressotypic cognitions,
behaviors, and affect and their deficient skills and styles place
them at elevated risk for developing depression.
Empirical support. The first component of Mechanism 3 postulates that depression in the parent is associated with negative
cognitions, overt behaviors, and affect. Depressed persons have
consistently been found to be characterized by more negative
cognitive functioning than have their nondepressed counterparts.
More specifically, depressed adults have been found to demonstrate negatively biased self-perceptions and cognitions, including
more internal, stable, and global attributions for negative events;
increased attention to, and memory for, negative stimuli; and high
levels of self-punishment and low levels of self-reinforcement and
self-efficacy (for reviews of this literature see Gotlib, Gilboa, &
Sommerfeld, in press; Gotlib & Neubauer, in press). Importantly,
depressed mothers' negative cognitions have been found to extend
to their parenting. They are more likely to endorse negative views
of themselves as parents (Gelfand & Teti, 1990; Goodman, Sewell,
Cooley, & Leavitt, 1993), to view themselves as having less
personal control over their children's development, and to see
themselves as less likely to be able to positively influence their
children (Kochanska, Radke-Yarrow, Kuczynski, & Friedman,
1987).
There is also ample evidence that depressed mothers expose
their children to depressive behaviors and affect. Researchers have
found, for example, that compared with nondepressed persons,
depressed individuals are more self-focused (Ingram, 1990; Pyszczynski & Greenberg, 1987), engage in more negative conversational content (Gotlib & Robinson, 1982; Kowalik & Gotlib,
1987), and demonstrate more negative behaviors in interactions
with others (Gotlib, 1982; Jacobson & Anderson, 1982). Depressed persons also elicit feelings of depression, anxiety, and
hostility in others with whom they interact (Gotlib & Meltzer,
1987). Perhaps not surprisingly, therefore, individuals have been
found to withdraw from interaction with depressed persons (cf.
Gurtman, 1986; see Gotlib & Whiffen, 1991, for a more detailed
review of this literature).
Similar observations have been made with respect to more
intimate interactions. For example, in interactions with their
spouses, which, presumably, the children have opportunities to
observe, depressed women have been found to engage in selfderogation, complaining, and dysfunctional problem-solving behavior and to exhibit elevated levels of hostility, anger, and conflict (e.g., Biglan et al., 1985; Gotlib & Whiffen, 1989; Hinchliffe,
Hooper, & Roberts, 1978). In extensive home observations, Hops
et al. (1987) found that depressed mothers' sadness was associated
with less aggressive affect of other family members; conversely,
family members' aggressive affect was observed to suppress the
mothers' dysphoric affect.
Finally, several researchers have examined more explicitly the
behaviors of depressed parents with their children (see Gotlib &
Goodman, 1999, for a review of this literature). Compared with
nondepressed psychiatric and nonpsychiatric controls, depressed
mothers have been observed in direct interactions with their children to display more sad and irritable affect (Cohn, Campbell,
Matias, & Hopkins, 1990; Hops et al., 1987; Radke-Yarrow &
Nottelmann, 1989); to be less positive, and more punitive, negative, and retaliatory with their children; to engage in more angry,
intrusive, hostile, and conflictual behavior (Field, Healy, Goldstein, & Guthertz, 1990; Goodman, Adamson, Riniti, & Cole,
1994; Hammen, 1991); and either to be ineffective in resolving
conflicts or to alternate between harsh, punitive discipline and lax
undercontrol (Dumas, Gibson, & Albin, 1989; Kochanska, Kuczynski, Radke-Yarrow, & Welsh, 1987).
It is clear, therefore, that depressed persons in general, and
depressed parents in particular, exhibit negative cognitions, behav-
RISK FOR PSYCHOPATHOLOGY
iors, and affect. The second component of Mechanism 3 contends
that these cognitions and behaviors make it more likely that the
depressed parent will be an inadequate social partner for the child
and will be unable to meet the child's social and emotional needs.
Given that children's parenting needs vary over the course of
development, the actual proposed pathways for this component
differ as a function of the age of the child at the time of the
maternal depression(s). For infants, two key aspects of parenting
are fostering an attachment relationship and facilitating the development of emotional self-regulation. Importantly, insensitive or
unresponsive parenting has been found to be among the strongest
predictors both of insecure attachment (e.g., Egeland & Farber,
1984) and of infants' difficulty in establishing effective selfregulation skills (Tronick & Gianino, 1986) and, further, may be
related to problems in infants' development of neuroregulatory
mechanisms (e.g., Dawson, Hessl, & Frey, 1994; Field, 1992). At
a more behavioral level, relative to their nondepressed counterparts, depressed mothers have been observed to provide lower
amounts of and lower quality stimulation for their infants (Livingood, Daen, & Smith, 1983); to be slower in responding, and less
contingently responsive, to their infants (Bettes, 1988; Field, 1984;
Field et al., 1990, 1985); and to use less reciprocal vocalization and
affectionate contact with their infants (Fleming, Ruble, Flett, &
Shaul, 1988).
For toddlers and preschool-aged children, parents must provide
the external support necessary for their children to develop an
accurate understanding of social and emotional situations (Cicchetti & Schneider-Rosen, 1986). The nature of this support includes providing their child with emotional language acquisition
and socialization (Gottman, Katz, & Hooven, 1996); guiding the
behaviors of their toddlers in social referencing situations (cf.
Campos & Steinberg, 1981; Walden & Ogan, 1988); facilitating
their children's relationships with peers and other adults, as well as
their involvement in extracurricular activities; and providing the
young child with adequate "scaffolding," that is, providing external, verbal support that facilitates a child's movement from one
developmental level of cognitive and social functioning to the next
(D. F. Goldsmith & Rogoff, 1995; Vygotsky, 1987). Toddlers or
preschool-aged children whose parents did not provide for these
needs would be predicted to have difficulties in the emergence of
effective autonomous functioning, in the management of emotionally arousing situations, and in their ability to organize and coordinate environmental resources (Cicchetti & Schneider-Rosen,
1986).
Investigators who have examined the interactions of depressed
mothers with their toddlers and preschool-aged children have
found that, compared with nondepressed controls, depressed mothers spend less time mutually engaged with their children in a
shared activity (D. F. Goldsmith & Rogoff, 1997). They also
initiate and terminate their children's attention to objects more
frequently, rather than encouraging sustained attention (Breznitz &
Friedman, 1988). When their children resist their attempts at
control, depressed mothers avoid confrontation, either immediately dropping their original demands or persisting at control but
failing to achieve a mutually negotiated compromise (Kochanska,
Kuczynski, et al., 1987). Finally, depressed mothers and their toddlers
and preschool-aged children have been found to engage in patterns of
coercive mutual interpersonal influence, including what are described
as retaliation and revenge (Kochanska, Kuczynski, & Maguire, 1989).
467
For school-aged children and adolescents, the stage-salient
needs shift to parents' provision of general social support or stress
buffering (i.e., helping their children to cope with other stressors;
cf. Lee & Gotlib, 1991b), helping their children to maintain their
focus on the cognitive-intellectual and social environment, and
monitoring their children's behavior and providing consistent discipline (Hops et al., 1987; Hops, Sherman, & Biglan, 1990; Patterson, 1982). Children whose parents fail to provide for these needs
would be expected to experience school failures and behavioral
and emotional problems. Interestingly, Hops et al. (1987) found
depressed mothers to suppress their dysphoric affect in response to
their children's aggressive affect, thereby reinforcing the children's misbehavior. Moreover, a number of investigators have
found that depressed mothers, compared with their nondepressed
counterparts, have more negative appraisals of, and lower tolerance for, their children's behaviors. Both of these variables, in
turn, have been found to be associated with more punitive parenting and might further be expected to be associated with higher
thresholds for rewarding behavior (e.g., Forehand, Lautenschlager,
Faust, & Graziano, 1986; Schaughency & Lahey, 1985). Finally,
depressed mothers have been observed to express more criticism
of their children, both in direct interactions with their children
(Hammen, Adrian, & Hiroto, 1988; Webster-Stratton & Hammond, 1988) and in interviews about their children (Goodman
et al., 1994).
We should note here that, consistent with a cognitive perspective on depression, several researchers have contended that depressed mothers' perceptions of their children's behaviors are
negatively distorted (e.g., Friedlander, Weiss, & Taylor, 1986;
Radke-Yarrow, Belmont, Nottelmann, & Bottomly, 1990; Rickard, Forehand, Wells, Griest, & McMahon, 1981). In contrast,
other researchers argue that depressed mothers are accurate reporters of their children's behavior (Conrad & Hammen, 1989; Richters & Pelligrini, 1989). It is important to note that these studies
may not reflect "accuracy" on the part of the mothers but, instead,
may be inadvertently capitalizing on a "match" of children's more
negative behaviors and depressed mothers' more negative response or reporting styles (cf. Coyne & Gotlib, 1983). As Richters
(1992) noted, studies are required examining whether depressed
mothers report more child behavior problems than are reflected by
independent, validated ratings of the same behaviors in the same
setting. More recently, using a large sample and sophisticated
methodology, Boyle and Pickles (1997) found that both maternal
depression and the associated family dysfunction or stress may
contribute to the mothers' negatively biased reports, especially
concerning their younger (5- to 7-year-olds), as opposed to older
(8- to 12-year-olds) children.
The results of studies of each developmental stage indicate,
therefore, that depressed parents are characterized by negative
perceptions of their children and by difficulties interacting with
their children and meeting the children's social and emotional
needs. The third component of Mechanism 3 maintains that this
problematic parenting would negatively affect the children's development of social and cognitive skills and styles. There are two
aspects of this component that are important. The first is whether
children of depressed mothers are in fact characterized by deficits
or delays in affective, behavioral, or cognitive skills or styles; the
second is whether these delays or deficits are related to the mothers' inadequate parenting.
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GOODMAN AND GOTLIB
What is the evidence that children of depressed mothers have
deficits or delays in affective, behavioral, or cognitive skills or
styles? Several investigators have reported findings consistent with
this component of the proposed mechanism. For example, researchers examining the attachment status and styles of infants of
depressed mothers have found that these infants are characterized
by insecure attachment (e.g., Radke-Yarrow, Cummings, Kuczynski, & Chapman, 1985; Teti, Gelfand, Messinger, & Isabella,
1995). More specifically, Teti et al. (1995) found greater levels of
insecure attachment, and specifically the Anxious Depressed
(Type AD) attachment classification, among preschoolers of depressed mothers (Type AD is identified by several depressive-like
features, including sad or flat affect, lethargy, or panic on separation, and an overall style of disorganization). Further, disorganized
attachment behavior in the infants has been found to be related to
the severity and chronicity of the mother's depression (Campbell
& Cohn, 1997; Teti et al., 1995).
Several investigators have documented the presence of other
types of deficits or delays in children of depressed mothers. Field
and colleagues (Field, 1994; Field, Pickens, et al., 1995), for
example, found that, compared with infants of nondepressed mothers, infants of depressed mothers showed delayed development of
autonomic regulation at 6 months, as evidenced by lower vagal
tone. Similarly, Dawson and her colleagues (e.g., Dawson, Grofer
Klinger, Panagiotides, Hill, & Spieker, 1992; Dawson et al., 1994)
found that infants of depressed mothers exhibit reduced left frontal
brain activity compared with infants of nondepressed mothers,
likely reflecting lower approach-related behavior. Compared with
toddlers of nondepressed mothers, children of depressed mothers
have been found to exhibit high levels of anxiety during a mildly
stressful situation (Radke-Yarrow & Sherman, 1985) and less
sustained attention to objects during spontaneous play with their
mothers (Breznitz & Friedman, 1988). Finally, Goodman, Brogan,
et al. (1993) found that 5- to 10-year-old children of mothers with
a history of unipolar depression were rated by their teachers as less
popular with peers than were children of well mothers. Thus
children of depressed mothers have been found to be characterized
by deficits or delays in affective, interpersonal, cognitive, and
bio-behavioral skills and styles.
The second aspect essential to the consideration that problematic parenting would negatively affect children's social and cognitive development is whether the biases, delays, or deficits that
have been identified in children of depressed mothers are related to
inadequate parenting. Most of the data that are relevant to this
question come from observations of mother-child interaction in
which the synchronies, contingencies, or patterns of behaviors
between the mothers and children are interpreted as reflecting the
consequences of inadequate parenting. For example, infants interacting with their depressed mothers, or with mothers who were
simulating depression and who were relatively unresponsive to the
infants, were found to exhibit predominantly negative affect in
their facial expression and gestures; the infants were observed
initially to persist in attempts to obtain the external regulation they
needed from their mothers, but they eventually began to engage in
self-directed regulatory behaviors (Gianino & Tronick, 1985;
Tronick & Gianino, 1986). Similarly, infants of depressed mothers
who were intrusive looked less at their mothers in interactions;
with depressed mothers who were withdrawn, infants protested
and appeared distressed (Cohn, Matias, Tronick, Connell, &
Lyons-Ruth, 1986; Tronick, 1989).
Conceptually similar findings have been obtained with older
children of depressed mothers. For example, reminiscent of Patterson's (1982) coercive family process model,5 Kochanska et al.
(1989) found that in a sample of mothers with a history of depression, negative maternal mood and the child's resistance to the
mother increased the likelihood of the mothers' aversive responses
to their children. Other investigators have observed children as
young as 2 years of age to engage in comforting behaviors in
response to their parent's distress (Dunn & Kendrick, 1981;
Radke-Yarrow, Zahn-Waxier, Richardson, Susman, & Martinez,
1994). In an analysis of the conditional responding of family
members to one another, Hops et al. (1987) found that the mother's
depressive behavior served to lower the probability that the children and husband would emit aggressive behavior; similarly, the
children's and husband's aggressive affect was found to suppress
the mother's dysphoric affect. Using causal modeling, Hammen,
Burge, and Stansbury (1990) found reciprocal associations between dysfunctional communication in the mother and negative
self-concept and interactional behavior in the children. Snyder
(1991) found support for a direct relationship between mothers'
distress (self-reported negative mood and stress) and their 4- to
5-year-old sons' conduct problems as well as a mediating role of
maternal discipline (more aversive behavior in response to the
child's aversive behavior and giving in to the child's aversive
behaviors). Finally, Goodman et al. (1994) found the expressed
negative attitudes of mothers toward their children to moderate the
association between maternal depression and children's lower
global self-worth. In sum, researchers using statistical modeling
and sequential analyses are beginning to provide support for a
direct role of depressed mothers' inadequate parenting in the
emergence of the children's maladaptive skills and styles.
The fourth component of Mechanism 3 maintains that, through
social learning or modeling, children acquire cognitions, behaviors, and affect that resemble that displayed by their depressed
mothers. In assessing the empirical support for this component of
the mechanism, we examine three literatures. First, we examine
evidence that children of depressed mothers themselves, even
though essentially asymptomatic, are characterized by negative
affect, behavior, and cognitions. Second, we assess correlational
studies that examine similarities between depressed mothers and
their children with respect to their affect, behavior, or cognitions.
Third, we examine evidence that modeling or other social learning
processes can explain the acquisition of these phenomena in the
children.
Are children of depressed mothers characterized by negative
affect, behavior, and cognitive functioning in the absence of explicit depressive symptoms? Children of depressed mothers have
been found in several studies to differ from control children with
respect to their negative affect and behavior. For example, compared with infants of well mothers and of psychiatric controls,
infants of both subclinically and clinically depressed mothers have
been found to be less responsive, less active, and less content; to
have flatter affect; and to show less distress during maternal
5
Patterson (1982) found an association between aggressive children and
a higher incidence of depression in the mothers.
RISK FOR PSYCHOPATHOLOGY
separation (e.g., Cohn et al., 1986; Dawson et al., 1992; Field et al.,
1985; Sameroff, Barocas, & Seifer, 1984; Whiffen & Gotlib, 1989;
Zekoski, O'Hara, & Wills, 1987; but see also Dawson, Frey,
Panagiotides, Osterling, & Hessl, 1997). Zahn-Waxler, Cummings, lannotti, and Radke-Yarrow (1984) found that, compared
with control children, 2-year-old children of depressed mothers
exhibited heightened emotionality when exposed to conflict and
distress in others, as well as a tendency to suppress their emotions
as a way of coping with stressful situations. School-aged and
adolescent offspring of depressed mothers have been found to have
poorer peer relations and less adequate peer relations skills than
have children of nondepressed control mothers (Beardslee,
Schultz, & Selman, 1987; Billings & Moos, 1985; Goodman,
Brogan, et al., 1993; Lee & Gotlib, 1989, 1991a).
In contrast to the number of studies of affect and behavior in
children of depressed mothers, surprisingly fewer empirical studies
were found to have shown that children of depressed mothers also
are characterized by negative cognitions. The presence of negative
cognitions in children of depressed mothers might reflect modeling
of their parents' negative thinking about themselves, or the experience of having been frequently criticized or reinforced for their
own negative views of the world. Most frequently, studies of
cognitive functioning in children focus on beliefs about the self.
Compared with children of well mothers, 8- to 18-year-old children of unipolar depressed mothers have been found to have
significantly lower self-concepts, to report a significantly more
negative cognitive style, to be more self-critical and more likely to
blame themselves for negative outcomes, and to be less likely to
recall positive self-descriptive adjectives (Garber & Robinson,
1997; Hirsch, Moos, & Reischl, 1985; Jaenicke et al., 1987).
Interestingly, Garber and Robinson (1997) found in a sample of
12-year-old children of mothers with a history of nonbipolar mood
disorders that these negative cognitions were stronger in offspring
of chronically depressed mothers, even after controlling for the
children's own depression scores. In one exception to this general
pattern, Goodman et al. (1994; Goodman, Brogan, et al., 1993)
found no significant differences between 5- to 7-year-old children
of mothers with a history of unipolar depression and children of
well mothers with respect to the children's self-perceived competence or locus of control beliefs; 8- to 10-year-old children differed
only on global self-worth.
Second, are the negative affect, behaviors, and cognitions of
depressed mothers associated with similar behaviors in their children? Observational studies of the infants and young children
interacting with their depressed mothers offer support for this part
of the mechanism. In several studies, Field and colleagues (Field et
al., 1990; Field, Healy, & LeBlanc, 1989) found that infants of
depressed mothers "match" their mother's negative state (interestingly, less matching was observed when the mothers were positive
toward the infants). Breznitz and Sherman (1987) found that young
children of depressed mothers match the low rates of speech of
their mothers in conversations with them. Similarly, Breznitz and
Friedman (1988) found that toddlers' duration of attention is
negatively correlated with the frequency of their mothers' shifts in
attention. Radke-Yarrow and Nottelmann (1989) found that toddlers and their depressed mothers display less mutually positive
affect and more mutually negative affect than do nondepressed
mother-child pairs, a pattern consistent with Hops et al.'s (1987)
findings described earlier, in which the valence of family mem-
469
bers' behaviors seemed to match that of the depressed mother.
Moreover, Radke-Yarrow, Belmont, Nottelmann, and Bottomly
(1990) found that negatively toned comments of depressed mothers were related to a measure of the children's negative selfschema. Somewhat contradictory with this pattern of findings was
Jaenicke et al.'s (1987) finding that, during problem-solving tasks,
mothers' and children's self-criticism levels were not significantly
associated with each other. Interestingly, however, maternal criticism of the child during these tasks was significantly correlated
with the children's self-critical comments during the tasks and
with the children's self-blaming style on a self-report measure of
attributional style.
Third, can the acquisition of these behaviors, affect, and cognitions in the children be explained by modeling or other social
learning processes? The reviewed studies provided useful information. If children match their mothers' negative affect, behavior,
and cognitions in the research settings, as they have been shown to
do, they most likely also do so at home. However, although the
evidence on children's matching of their depressed mothers' dysphoric affect, behavior, and cognitions is consistent with social
cognitive theory, stronger support would come from tests of Bandura's (1986) tenets regarding variables that should influence the
likelihood of modeling. For example, based on those tenets we
would expect mothers to be stronger models for girls than for boys.
In fact, two studies have demonstrated that depressed mothers may
be more powerful models for their daughters than for their sons.
Hops et al. (1990) found that 11- to 16-year-old daughters of
depressed mothers exhibited more dysphoric affect and less happy
affect than did younger (3- to 10-year-old) girls or boys of either
age, and at levels similar to those displayed by their mothers.
Similarly, Radke-Yarrow and Nottelmann (1989) found that
daughters of unipolar depressed mothers were more likely to
match their mothers' downcast mood than were their sons. These
analyses of behavioral synchrony suggest the operation of early
socialization of negative mood in daughters of depressed mothers
to a greater extent than is the case in sons.
Another tenet that might be abstracted from Bandura's (1986)
formulations is that boys would be expected more so than girls to
model the anger-aggressive component of their mothers' depression, whereas girls would be more likely to model the behaviors
more compatible with the stereotypical feminine gender role, such
as dysphoric mood and ruminative thinking. We found no published reports of research testing this tenet. In an unpublished
paper, Kochanska (1987) reported finding that although well
women demonstrated the predicted pattern of being more tolerant
and supportive of their sons' than their daughters' anger, the
pattern was reversed for depressed mothers. Further research on
this tenet is needed.
In sum, the data on children's matching of their depressed
mothers' dysphoric and angry affect, behavior, and cognition
support Bandura's social cognitive theory of how children of
depressed mothers are influenced, whether through modeling, direct instruction, or performance outcomes. However, although
these findings are consistent with a modeling or other social
learning mediation mechanism, it is important to note that they are
not inconsistent with other explanations.
The fifth and final component of Mechanism 3 maintains that
the children's deficient skills and styles, and their acquired depressotypic cognitions, behaviors, and affect, place them at elevated
470
GOODMAN AND GOTLIB
risk for developing depression. That is, are these styles, cognitions,
behaviors, and affect associated with an increase in the children's
risk for the development of depression or other disorders? Some of
the evidence relevant to this question comes from studies using
samples unselected for level of maternal depression. For example,
researchers have demonstrated that infants with lower vagal tone
vocalize less, have less optimal neurological development, show
less facial emotional reaction and expression, are less attentive to
the environment, are less able to self-soothe, and have higher
cortisol levels, suggestive of the experience of greater stress (e.g.,
Field, Pickens, et al., 1995; Forges, 1992; Forges, DoussardRoosevelt, & Maiti, 1994); moreover, Portales, DoussardRoosevelt, Lee, and Forges (1992) found that inability to suppress
vagal tone during attention-demanding situations at 9 months of
age predicted behavior problems at 3 years. We noted above that
Dawson and her colleagues found that infants of depressed mothers exhibit reduced left frontal brain activity. Other investigators
have documented that this asymmetric pattern of lower left frontal
activity is associated with a vulnerability to experience and express
negative affect in stressful situations, with a tendency to withdraw
and avoid interaction, and with lower behavioral initiation (Davidson & Fox, 1988; Fox, 1994; Gotlib, Ranganath, et al., 1998).
Finally, several investigators have found that negative affect is
related to subsequent learning difficulties (e.g., Bugental, Blue,
Cortez, Fleck, & Rodriguez, 1992; Singer & Fagen, 1992).
Focusing more explicitly on depression, investigators have
found that compared with well mothers, depressed mothers use
more negative and less productive communications with their
children during a conflict task. Moreover, Hammen (1991) found
that aspects of the mothers' communications with their children
were significantly associated not only concurrently with children's
diagnoses, behavior problems, social competence, and academic
performance but prospectively with affective diagnoses at a
6-month follow-up.
With respect to children's negative cognitive functioning, it is
not clear even in the general population whether these negative
cognitions precede the development of depressive disorders and
play a causal role in depression (cf. Barnett & Gotlib, 1988; Gotlib
& Krasnoperova, 1998). In a meta-analysis of seven studies, Joiner
and Wagner (1995) found moderate support for overall negative
attributional style as a prospective predictor of increases in depressive symptoms in children. Only one study was found to have
tested prospectively the predicted relation between negative cognition and subsequent depression in the children of depressed
mothers. Hammen et al. (1988) found that, among children of
depressed mothers, negative cognitions about the self (self-concept
and negative self-schemata), but not negative attributional style,
predicted adjustment problems at a 6-month follow-up assessment.
No study has found that negative cognitions predict a diagnosis of
depression in children of depressed mothers.
Finally, it is important to note that the presence of a mechanism
linking the early stress of inadequate parenting and the subsequent
development and expression of depression in the child is supported
by results from animal studies. For example, Ladd, Owens, and
Nemeroff (1996) exposed rat pups to the stress of separation from
their mothers for 6 hr/day from age 6 days to 3 weeks. The
separated rat pups were found to produce twice as much CRF as
did pups who were not stressed. Moreover, as adults, the rats that
had experienced separation produced 25% more adrenocortico-
tropic hormone (ACTH) in reaction to stress (a mild foot shock).
Thus, rats stressed by maternal separation as pups were found as
adults to overreact to stress. Ladd et al. proposed that the overproduction of CRF is related to hyperactivity of the HPA axis,
which, in turn, is related to a predisposition to depression. It is
important to note, however, that this pattern may not hold for
childhood depression. Ryan and Dahl (1993) reported that, in at
least some clinically depressed children (ages 8-12 years), ACTH
may be down-regulated in response to CRF challenges, perhaps
explaining the normal concentrations of cortisol that have been
observed in depressed children and adolescents.
Summary. There is little question that depressed mothers are
characterized by negative cognitions, overt behaviors, and affect.
This depressive functioning not only renders the depressed mother
an inadequate social partner for her children but, further, leaves her
unable to meet her children's social and emotional needs. These
unmet needs, in turn, limit the children's development of social
and cognitive skills. Moreover, children of depressed mothers are
clearly exposed to the mothers' depressive cognitions, behaviors,
and affect. Consequently, these children, from infants through
adolescents, have been found to exhibit cognitive functioning,
affect, and behaviors that mirror broadly the depressed mothers'
functioning. Although there are few studies that have examined the
hypothesis that these negative behaviors, affect, and cognitions in
offspring of depressed mothers are a precursor to the development
of depression, there is intriguing evidence, from both human and
animal studies, that this negative functioning in both the mothers
and the children may indeed place the children at elevated risk for
experiencing depression.
Mechanism 4: The Context of the Lives of Children in
Families With Depressed Mothers, Particularly the
Stressors, Contributes Significantly to the Development
of Psychopathology in the Children
Researchers have documented a strong and consistent association between stress and depression in adults (e.g., Billings &
Moos, 1982; Gotlib & Hammen, 1992; Hammen, 1988). Recently,
investigators have attempted to elucidate the nature of this association by delineating more specifically different aspects of both
stress and depression. For example, Hammen (1991) made an
important distinction between dependent and independent stressors
and, further, demonstrated that the negative life events experienced
by depressed adults may actually be a consequence, rather than a
cause, of their depression. Most relevant here is that children of
depressed mothers are exposed not only to their mother's depression but also to a variety of stressors that are associated with the
depression; it is the children's exposure to these stressors that is
hypothesized in this mechanism to mediate the association between maternal depression and child psychopathology.
Empirical support. Because few researchers have examined
contextual variables in their studies of children of depressed mothers, we know little about how children of depressed mothers deal
with the relatively high number of stressors to which they are
exposed. There is little question that children of depressed mothers
are, in fact, exposed to a greater number of stressors in their lives
than are children of nondepressed mothers. For example, Hammen
et al. (1987) found that families with unipolar depressed mothers
reported higher levels of stress than did families with medically ill
RISK FOR PSYCHOPATHOLOGY
mothers and families with well mothers. More specifically, families with unipolar depressed mothers reported more stress in the
domains of marital and social relationships, job, finances, and
relations with children. In addition, children in families in which
there was a depressed mother reported significantly more episodic
and chronic stressors than did children with well mothers (Adrian
& Hammen, 1990, reported in Hammen, 1991).
Perhaps the most pervasive stressor to which children of depressed mothers are exposed is parental marital discord. The
association between marital discord and depression has been well
documented (e.g., Bruce & Kim, 1992; Crowther, 1985). Depressed persons' marital relationships have been consistently characterized as conflictual, tense, and hostile (e.g., Gotlib & Beach,
1995; Kowalik & Gotlib, 1987), and interactions between depressed women and their husbands are markedly negative (e.g.,
Hautzinger, Linden, & Hoffman, 1982; Ruscher & Gotlib, 1988).
Although the direction of effect in the association between marital
discord and depression is unclear (it is most likely to be reciprocal;
cf. Gotlib & Hooley, 1988; Hammen, 1992; Rutter & Quinton,
1984; but see also Gotlib, Lewinsohn, & Seeley, 1998), for the
purposes of this article the important point is that children of
depressed mothers are almost certainly exposed to high levels of
marital conflict. Indeed, Gotlib (Gotlib & Avison, 1993; Gotlib &
Lee, 1990) has argued specifically that the elevated marital discord
associated with maternal depression may mediate the adverse
impact of maternal depression on children.
Consistent with this formulation, Fendrich, Warner, and Weissman (1990) and Goodman, Brogan, et al. (1993) both reported data
supporting the prediction that marital discord exacerbates the
negative effects of maternal depression on child functioning. More
specifically, among children with depressed mothers, those whose
parents were divorced were more likely to be rated by their
teachers as undercontrolled and lower on ego resiliency (Goodman, Brogan, et al., 1993) and to have a conduct disorder (Fendrich et al., 1990). Interestingly, investigators who have attempted
to separate the contribution of marital discord and maternal depression to children's adverse outcomes have generally found that
marital discord is more strongly related to children's problems
than is maternal depression (e.g., Caplan, 1989; Cox, Puckering,
Pound, & Mills, 1987; Emery, Weintraub, & Neale, 1982). Indeed,
the consistency of this finding has led some theorists to suggest
that heightened marital anger and hostility mediate the association
between parental mental illness and children's psychological disturbance (e.g., Rutter & Quinton, 1984).
Finally, a small number of investigators have examined stressors
other than marital discord that might at least partially explain the
adverse outcomes experienced by children of depressed mothers.
For example, Belle (1982) and Pound, Cox, Puckering, and Mills
(1985) reported that both maternal depression and stress associated
with poverty were significant predictors of problems in the children. Similarly, Billings and Moos (1983) found that children
whose depressed mothers reported high levels of stressful life
events had more adjustment problems than did children whose
depressed mothers reported low levels of stress. Hammen et al.
(1987) found that both chronic stress and current depression (but
not lifetime history of depressive disorder) uniquely contributed to
the prediction of children's diagnostic status and behavior
problems.
Summary. In sum, there is little question that children of
471
depressed mothers are exposed not only to their mothers' depression but also to a more stressful environment than that experienced
by children of nondepressed mothers. Despite the consistency of
this general finding, little research has examined specifically the
potential mediating role of stress in the association of maternal
depression and the development of depression or behavior problems in the children. Indeed, few investigators have included
contextual variables in their studies of the children of depressed
mothers. One important caution that arises from a consideration of
stress as a possible mediator of the association of maternal depression and adverse child outcome is that investigators who do not
assess (or control for) stressors experienced by depressed mothers
and their children may be overestimating the specific effect of the
mother's depression on their children's difficulties. It may be that
chronic stress should be treated as a separate and important predictor of outcome in children with depressed mothers (cf. Hammen, 1991). We return to this point in greater detail later in this
article.
Moderators
What characteristics of children, the depressed mother, or the
family, and what other aspects of the environment affect the nature
of the association between maternal depression and negative child
outcome? Is there support for factors that increase or decrease the
risk for the child? Are there subgroups of children of depressed
mothers who are at particularly elevated risk? In this section we
address questions about the role of the father, critical periods, and
level of "exposure."
Moderator 1: Fathers May Increase the Risk for
Psychopathology in Children of Depressed Mothers If
They Are Absent or If They Also Have Psychopathology.
Similarly, Fathers May Represent a Protective Factor
If They Are Healthy, Involved, and Supportive
Empirical support. Generally, the risk literature has documented the positive role of a supportive adult in increasing the
resilience of children at risk for psychopathology (Garmezy, 1985;
Werner & Smith, 1980). Less attention has been paid more specifically to the role of healthy adults in the lives of children with
depressed mothers. Indeed, studies that have included fathers have
done so most typically to provide information concerning assortative mating. Assortative mating increases the likelihood that the
spouse of a depressed mother also has a depressive disorder or
another form of psychopathology (cf. Gotlib & Hammen, 1992;
Merikangas, 1984; Merikangas, Prusoff, & Weissman, 1988).
Consequently, children with a depressed mother are likely to also
have a father with emotional disturbance.
There are several ways in which fathers could either exacerbate
or attenuate the effects of maternal depression on child functioning. For example, a father with depression or some other disorder
could increase the risk for psychopathology in the offspring
through both genetic and environmental factors. On the other hand,
healthy fathers who are involved in their children's lives could
provide a positive role model for their children, as well as substitute or respite caregiving for the children; fathers could also offer
support for the depressed mothers, who could then in turn provide
better quality parenting to their children (Belsky, 1984).
472
GOODMAN AND GOTLIB
A number of researchers have obtained support for the prediction that the father's functioning may moderate the association
between maternal depression and child dysfunction. Weissman et
al. (1984) found that children with two depressed parents are at
significantly greater risk for disorder than are children with one
depressed parent. Goodman, Brogan, et al. (1993) found that
fathers' psychiatric status, along with parents' marital status, explained a significant proportion of the variance in the social and
emotional competence of 6- to 10-year-old children of clinically
depressed mothers. Similarly, Conrad and Hammen (1989) found
that the presence of a healthy father in the home was associated
with lower rates of disorder among school-aged children of depressed mothers. Eiden and Leonard (1996) found that infants of
mothers who were depressed and who also had partners who
engaged in heavy drinking were even more likely to be classified
as insecurely attached than were infants of depressed mothers
whose partners did not drink heavily. Finally, Thomas and Forehand (1991) found that fathers' depression scores added small but
significant unique variance, beyond that accounted for by maternal
depression, in adolescents' teacher-reported emotional or behavioral problems.
' Cairo, Grant, Gotlib, and Compas (1993) examined maternal
and paternal characteristics at 1 month postpartum as risk and
protective factors for children's internalizing and externalizing
problems at 2-3 years of age. Although a low level of depressive
symptoms in the husbands of depressed mothers was not found to
function as a protective factor for the children's problems, fathers'
depressive symptoms did serve to increase the mothers' depressive
symptoms measured when the children were 2-3 years old. Thus,
fathers' depression may affect the children indirectly by exacerbating the mothers' depression.
Some researchers have examined the processes by which the
quality of the father's functioning may moderate the association
between maternal depression and child functioning. Hops et al.
(1987), for example, conducted sequential analyses on family
interactions and found higher rates of caring behavior directed to
3- to 16-year-old children by psychiatrically well husbands of
depressed wives than by psychiatrically well husbands of nondepressed wives. In a similar study with younger children, Hossain et
al. (1994) found that nondepressed fathers had more positive
interactions with their 3- to 6-month-old infants than did their
depressed wives. Indeed, the well fathers were rated as significantly higher than the depressed mothers on scales of affective
state, facial expressions, vocalizations, and game playing. The
infants exhibited higher quality interactions with the fathers than
with their depressed mothers. This finding suggests that husbands
whose wives are depressed are attempting to compensate for the
more negative behavior of their wives and are being more positive
in their interactions with their children. Although Chabrol, Bron,
and Le Camus (1996) failed to replicate these findings, they may
have been hampered by a small sample size (N = 10) and relatively low levels of depressive symptoms in their sample.
Summary. Evidence is accumulating that fathers play an important role in families with depressed mothers, either exacerbating the risk of psychopathology in the child or protecting the child
from the adverse effects of maternal depression. Although we
found direct support for the moderating effect of the father in
several studies, the results of other investigations suggest that the
relation may be more complex. Transactional patterns were de-
scribed from sequential observations both of family interactions in
homes (Hops et al., 1987) and of infants interacting with their
depressed mother and well father (Hossain et al., 1994). More
studies will be needed to elucidate the nature of the role both of
fathers who are well and of fathers who are emotionally distressed.
Moderator 2: The Timing and Course of Mothers'
Depression Will Moderate the Association Between
Maternal Depression and Negative Outcomes
in the Children
Based on our general knowledge of child development, it is
almost certain that first exposure to maternal depression will have
a stronger and more negative impact when children are younger
than when they are older. Although serious questions have been
raised about the validity of the initial concept of a critical period
(e.g., Turkewitz & Devenny, 1993), research examining early
physiological, affective, and cognitive development has indicated
that these systems continue to develop rapidly over the first few
years of life and that perturbations have consequences for subsequent development. For example, studies examining neurophysiological development have documented that the systems that are
relevant to the regulation of arousal are functionally immature at
birth and mature gradually during the first few years of life. More
specifically, the lability of organismic arousal declines during the
first year of life with the maturation of the HPA system and
parasympathetic regulation (as indexed by vagal tone; Stansbury &
Gunnar, 1994; Forges et al., 1994). At the same time, cortical
inhibitory controls over arousal are gradually emerging (Dawson,
1994; Rothbart, Ziaie, & O'Boyle, 1992). Thus, mothers' regulation of infants' emotions is needed most in this first year of life; the
presence of postpartum depression may render depressed mothers
incapable of providing this guidance.
Another consequence of early exposure to maternal depression
is that it may be difficult for a young child to recover from the
negative effects of a mother's depression; thus, the negative effects
could continue through later periods of the child's development.
Although the mother's depression is likely to remit, at least temporarily, we know little about malleability of the early physiological, cognitive, affective, and behavioral patterns acquired by the
child. Moreover, given early negative effects of maternal depression, the child will have lost ground, relative to his or her peers, in
the course of normal development (e.g., in the mastery of some
stage-salient social skills), which will put him or her at a disadvantage (Hay, 1997; L. Murray & Cooper, 1997). Similarly, the
child may also have acquired a peer status (e.g., rejected or
neglected) that is difficult to alter. Finally, dysfunctional behavioral patterns may be established, as may the beginnings of negative cognitive sets, beliefs, and so on.
A related matter in considering the relationship between depressed mothers and their children is that behavioral patterns that
were adaptive for the children in the short term in dealing with the
mothers' depressive episodes may generalize to other contexts,
evolving into maladaptive behavior patterns. For example, a response pattern of withdrawal may be adaptive in the context of
inconsistent, unresponsive, or harsh parenting that characterizes
currently depressed mothers. However, the child might fail to
discriminate improvements in the parent's behavior or to identify
RISK FOR PSYCHOPATHOLOGY
positive opportunities for interaction with other family members,
peers, or other adults.
Finally, and implicit in this discussion, the second part of
Moderator 2 maintains that a more chronic course of depression
will have a more adverse impact on children's functioning than
will a single episode of depression. As we noted earlier, depression
is typically a recurrent disorder, with over 80% of depressed
patients experiencing more than one depressive episode (e.g.,
Belsher & Costello, 1988; Mueller et al., 1996). Nevertheless, in
any sample of depressed mothers there will be considerable variability in course of the women's depression, and it is likely that the
chronicity of the mother's depression will moderate its impact on
the child.
Empirical support. Despite the strong theoretical and conceptual basis for Moderator 2, the empirical support is weak. With
respect to the possible differential effects of earlier versus later
exposure to maternal depression, no studies have compared children who vary in their age of first exposure. Similarly, few studies
have tested the hypothesis that a chronic or episodic course of
maternal depression will have more negative consequences for the
children than will a single depressive episode. Sameroff, Seifer,
Zax, and Barocas (1987) found chronicity to contribute to the
prediction of developmental course in children with depressed
mothers. Similarly, Campbell, Cohn, and Meyers (1995) found
that women whose depressions were chronic from 2 months
through 6 months postpartum had infants who were less positive
during face-to-face interaction than did women whose depressions
were episodic, although interestingly, chronicity was unrelated to
security of attachment (Campbell & Cohn, 1997). Beardslee and
his colleagues (e.g., Beardslee et al., 1987; Keller et al., 1986)
found that the chronicity of parents' affective disorder was related
to lower adaptive functioning and higher rates of psychopathology
in their adolescent children. In a related study, Hammen et al.
(1991) reported a strong temporal association of maternal depression episodes and the child's diagnosis for 11 children who developed major depression.
Another group of investigators took a slightly different perspective on the proposed moderator, examining whether a reduction in the parents' depressive symptomatology results in a
return to a normal level of functioning in the children. Field
(1992) examined 6-month-old infants of mothers who had been
depressed early in the infants' lives but were no longer depressed. Field noted that the infants no longer looked "depressed" at 6 months, nor did they exhibit cognitive delays or
emotional symptoms at 12 months of age. Other researchers
have reported more broadly that children's functioning improves when family adversities, not specifically parental depression, decrease (e.g., Cicchetti & Schneider-Rosen, 1986;
Pianta, Erickson, Wagner, Kreutzer, & Egeland, 1990).
In contrast to these findings, however, several other longitudinal studies found that children of depressed mothers continue
to have behavior problems following the mothers' recovery. For
example, both Billings and Moos (1985), in a 1-year follow-up
of children who had ranged in age from 3 to 18 years old, and
Cox et al. (1987), in a 6-month follow-up of 2-year-olds, found
that depressed parents who had remitted continued to report
more dysfunction in their children than did the control parents,
although less than the nonremitted group. Alpern and LyonsRuth (1993) followed low-income 4- to 6-year-old children
473
whose mothers had been depressed when the children were 18
months old. These investigators found that regardless of
whether the mother had recovered, children who were 18
months old at the time their mothers had been depressed had
higher parent- and teacher-rated child behavior problems than
did children of never-depressed mothers (unfortunately, there
were no explicit comparisons of the continuously depressed
with the recovered group). Similarly, maternal depression when
children were 14 months old or younger has been found to
predict preschool-aged children's behavior problems (Ghodsian, Zajicek, & Wolkind, 1984) and 4-year-olds' lower cognitive ability (Cogill, Caplan, Alexandra, Robson, & Kumar,
1986), regardless of the mother's depression status at followup. Stein et al. (1991) found that postpartum depression had a
negative effect on 19-month-old children even when their mothers' depression had remitted. Finally, Lee and Gotlib (199la)
reported a 10-month follow-up of 7- to 13-year-old children of
both depressed and nondepressed patients and community controls. Lee and Gotlib's results indicated that the group of
formerly depressed women, despite a significant reduction in
their depressive symptoms, continued to describe their children
as having a greater number of behavior problems (both internalizing and externalizing) than did the nondepressed control
mothers. Importantly, clinical interviews with these children
also revealed high levels of mood symptoms and somatic
complaints.
Finally, we should acknowledge the possibility that some of the
correlates of maternal depression, such as the deficits in parenting
by depressed mothers, marital distress, and so on persist beyond
the depressive episode itself and may explain the residual difficulties in the children following the mothers' recovery. Consistent
with this possibility, Stein et al. (1991) found that mothers whose
postpartum depression had remitted continued to engage in less
affective communication and sharing with their 19-month-old toddlers than did mothers with no history of depression. In contrast,
however, Campbell and Cohn (1997) found no evidence of dysfunctional qualities of mother-infant interaction among mothers
who were no longer clinically depressed, even if they were continuing to experience and exhibit low levels of depressive
symptoms.
Summary. We found no studies that examined whether earlier
exposure to maternal depression has more adverse effects on
children than does later exposure. Results from the few follow-up
studies are more relevant to the concern about whether infants and
young children recover from deficits associated with early exposure to a depressed mother. For the most part, these studies found
that although there is some level of recovery, the children do not
function as well as children who had not had the early exposure.
Moreover, although chronicity of maternal depression appears to
be an important component of this model, it is clear that much
more research is necessary to elucidate the impact on children of
more chronic forms of maternal depression. Unfortunately, investigators examining the effects of maternal depression on child
functioning rarely provide information concerning the course of
the mothers' depression; similarly, there are virtually no studies
that have treated chronicity of maternal depression as a variable of
interest. Longitudinal studies would be most useful in this regard,
given their relative independence from biases in retrospective
reporting on course or in psychiatric history records.
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GOODMAN AND GOTLIB
Moderator 3: Characteristics of the Children, Such as
Temperament, Gender, and Intellectual and SocialCognitive Skills, Moderate the Association of Maternal
Depression and Negative Child Outcomes
Transactional considerations raise the question of whether some
children are more vulnerable than others to the interpersonal
contexts of depression or to the biological risks associated with
this disorder (i.e., the dysfunctional neuroregulatory mechanism
described above). For example, children with easier temperaments
are expected to be less vulnerable to the effects of the inadequate
parenting that has been observed in depressed mothers (Bates,
Maslin, & Frankel, 1985; Cutrona & Troutman, 1986). This decreased vulnerability is predicted to be a function of the children's
lower sensitivity to change, higher threshold for stimulation, and
more flexible response style (i.e., less reactivity to environmental
challenges); such children are also less of a stressor to already
stressed parents. More broadly, children may vary in stressresistance or coping styles, and these individual differences are
hypothesized to moderate the biological, parenting, and stress
exposure effects of maternal depression.
Empirical support. Unfortunately, we found no studies that
lend support to this potential moderating role of temperament in
the association between maternal depression and child dysfunction. Somewhat tangentially, some investigators have found that
mothers' perceptions of their infants as being difficult to care for
are associated with their levels of depression (Cutrona & Troutman, 1986; Gotlib, Whiffen, Wallace, & Mount, 1991). Clearly,
this is a critical area for further research, particularly in light of
recent findings suggesting a neuroregulatory basis for temperament (e.g., Kagan et al., 1988) and a predictive role of childhood
temperament for adolescent psychopathology (e.g., Schwartz,
Snidman, & Kagan, 1996).
Another characteristic that has been proposed to moderate the
association of maternal depression and child psychopathology is
the gender of the child. Girls may be more vulnerable than boys to
the effects of maternal depression because of gender role modeling, especially during adolescence (Hops, 1996). It is also possible
that girls and boys are affected by maternal depression in different
ways. For example, whereas daughters of depressed mothers may
be more vulnerable to develop depression, sons of depressed
mothers may be more likely to develop conduct problems (Cummings & Davies, 1994). Furthermore, given the greater fetal and
neonatal mortality in boys than girls, it is also possible that boys
are more vulnerable than are girls to the hazards of the in utero
environment. Finally, boys may have stronger biological reactions
to stress than do girls, although this position is controversial (e.g.,
Emory, Schlackman, & Fiano, 1996).
The findings on gender differences in psychiatric outcomes have
been mixed. Research has shown that, in general, boys are at
higher risk than girls for the development of psychopathology
(Rutter & Quinton, 1984), although this pattern may be reversed at
adolescence (Petersen, 1988). Among investigators who have examined children of depressed mothers, most either did not report
gender differences or reported them not to be significant (e.g.,
Hammen, 1991; Harnish, Dodge, Valente, & Conduct Problems
Prevention Research, 1995; Thomas, Forehand, & Neighbors,
1995). And among those studies in which significant gender differences have been obtained with respect to the presence of psy-
chopathology in the offspring of depressed mothers, some have
found girls to be worse off than boys (e.g., Davies & Windle,
1997; Fergusson, Horwood, & Lynskey, 1995; Hops, 1996; Keller
et al., 1986), while others have found boys to function more poorly
than girls (e.g., Gross, Conrad, Fogg, Willis, & Garvey, 1995; L.
Murray, Fiori-Cowley, Hooper, & Cooper, 1996; Sharp et al.,
1995). Hay (1997) reported that in one sample of postpartum
depressed mothers, depression was associated with lower cognitive
scores for boys but not for girls; this pattern was not replicated,
however, in another sample of postpartum depressed mothers.
It is likely that different models may be necessary to understand
the differential risk to sons and daughters of depressed mothers.
Hay (1997) suggested that infant boys may be more vulnerable
than girls to mothers' noncontingent responsiveness and negative
affect, as evidenced by their being more likely to develop insecure
attachments (L. Murray, 1992). Klimes-Dougan and Bolger (1998)
found differences in the coping strategies of sons and daughters of
depressed mothers. K. T. Murray and Sines (1996) found that
although both genetic and nonshared environmental factors accounted for significant proportions of the variance in children's
depressive symptomatology, the relative contributions and the
nature of the environmental factors differed for boys and girls.
A final possible moderator of the association between maternal
depression and child psychopathology is children's intelligence or
level of social-cognitive skills. Children of depressed mothers may
be protected against adverse outcome concurrently and prospectively if they are more intelligent (Radke-Yarrow & Sherman,
1990) or have better social-cognitive skills (Beardslee et al., 1987;
Downey & Walker, 1989). For example, Radke-Yarrow and Sherman (1990) found that among 5- to 6-year-old children of depressed mothers who were characterized by three protective factors (having above average intelligence, being socially engaging,
and having a "special positive place in their families"), none met
criteria for a psychiatric diagnosis. The 8- to 11-year-old children
in the same families who had this set of protective factors were
also less likely to have psychiatric disorder.
Two studies offer limited support for a role of social-cognitive
functioning as a mediator of the association between maternal
depression and child functioning. Beardslee et al. (1987) found
that adolescents' interpersonal competence, measured by their
social-cognitive capacity for mutuality in relationships, added a
small but significant amount of explained variance in predicting
their level of functioning, even after accounting for age, sex, IQ,
parents' illness, and disorder in the adolescent. Unfortunately, the
authors were unable to examine possible differential effects of the
timing of parents' depressions and how that might be related to the
adolescents' development of social-cognitive skills. In the second
study, Downey and Walker (1989) found that interpersonal
problem-solving competence and attributional and response biases
of 9- to 14-year-old children reduced their risk of aggression and
peer rejection, but only among the subset of children who were
maltreated by their clinically depressed mothers.
Summary. The results of a relatively small number of studies
offer limited support for the role of child temperament, gender, and
intellectual and social-cognitive skills as moderators of the association between maternal depression and child dysfunction. Although some child characteristics are intriguing for their potential
to function as protective factors, others such as low intelligence
and poor social-cognitive skills may represent early manifestations
RISK FOR PSYCHOPATHOLOGY
of psychopathology in the children, the vulnerabilities in our
model. For example, the poor attention and concentration associated with depression could contribute to lower IQ test scores.
Similarly, children with poor social-cognitive skills are more likely
to be rejected and may behave aggressively, thereby increasing
their risk for psychopathology (Dodge, 1990; Rubin, Hymel, Mills,
& Rose-Krasnor, 1991). Thus, although there is preliminary support for the inclusion of these variables, and of child gender, in our
model, the role of these variables is not yet clear, and alternative
hypotheses must be tested.
Issues and Recommendations
In this article, we have proposed a model of the transmission of
risk to children of depressed mothers. A major purpose of this
model is to guide our understanding of the specific multiple
processes that might explain the adverse outcomes of the offspring
of depressed mothers, account for how these risk mechanisms
might interact, and consider the role of development in the transmission of risk. In presenting this model we reviewed a large
number of studies, many of which provided support for specific
components of the model. In this section we raise and discuss four
issues that we believe are particularly relevant to this model: (a)
the strengths and limitations of the proposed mechanisms, (b) the
level of theory that best serves this area of study, (c) the specificity
of the model to depression in the mothers and as the adverse
outcome to the children and the consideration needed for the
potential role of specific correlates of maternal depression, and (d)
the importance of the concept of sensitive periods and children's
recovery from adversity. In presenting this discussion, we also
offer specific suggestions for future research that we believe would
be important in beginning to address and resolve these issues.
Strengths and Limitations of the Proposed Mechanisms
In assessing the relative strengths of the various components of
the model of risk that we have presented in this article, we present
an evaluation of the research described earlier in the context of the
four risk mechanisms. Where possible, we examine the strength of
the evidence that the proposed mechanisms mediate the association between maternal depression and psychopathology in the
child. Although none of the mechanisms or moderators proposed
in the model can be considered to have been supported conclusively, support for some components of the model is more robust
than for others, and in this section we evaluate the strength of this
support. We also discuss evidence for a developmental course of
risk, whereby the effects of the mechanisms may be different for
children of different ages, or as a related point, may be a function
of the timing of the mother's depression. We turn now to a brief
evaluation of the empirical support for the four proposed mechanisms of the transmission of risk to children of depressed mothers.
Genetics mechanisms. The genetics mechanism has received
strong support with respect to both depression in adults (although
not specifically for children of depressed parents) and the heritability of traits and environmental factors that increase vulnerability
to depression. There is less clear support for the genetic contribution to depression that is postulated to emerge during childhood or
adolescence among children of depressed mothers. In addition,
although trait markers for depression in children have been pos-
475
tulated, they have not yet been identified (Puig-Antich, 1984;
Puig-Antich et al., 1983).
There are also a number of problems in the genetic approach to
risk for depression that have not yet been resolved. Most important
is that we do not yet know exactly what is inherited and how that
inheritance might be manifested—answers to these questions are
essential in attempting to understand the functioning of children of
depressed parents. From a more methodological perspective, most
of the family studies have used clinical samples, which could
confound their results. That is, depressed mothers may be more
inclined than nondepressed mothers to bring their depressed children for treatment (Goodman et al., 1997), biasing the findings
toward increased rates of depression in the relatives. Studies of
twins, adoptees, and step-siblings have the advantage of having
sampled from an unselected population rather than from clinical
samples. Nevertheless, these children and their families are not
representative of the general population of children, which raises
important questions concerning the generalizability of these findings (cf. Baumrind, 1993; Hoffman, 1985, 1994; Plomin &
Daniels, 1987).
Issues of reliability and validity of measurement are also particularly important with respect to genetic mechanisms of risk. It is
critical, for example, that investigators develop reliable and valid
measures of the environment of children of depressed mothers and
critical that they use measures and classification procedures that
have already been demonstrated to be reliable and valid in the
assessment of depression in both parents and their children. Studies in this area have also varied widely with respect to the informant that they used to assess children's symptoms of depression,
sometimes relying solely on the relatively insensitive parent report
and, in any case, limiting the ease with which we can compare
findings across studies (e.g., Angold et al., 1987). More broadly,
investigators will need to examine genetic and environmental
influences using experimental designs that overcome the weaknesses of established behavior genetics designs, for example, the
"equal environments" assumption with respect to monozygotic and
dizygotic twins and adopted and biological children (Hoffman,
1985, 1994); investigators will also need to develop designs that
are more sensitive to socialization models and environmental
theory (e.g., Bronfenbrenner & Ceci, 1994; Hoffman, 1985) and
develop measures of family environment that are less dependent
on questionnaires.
Finally, behavior genetics research designs typically ignore important developmental and transactional considerations. A separate
analysis by the age of the children is not sufficient to address
developmental concerns. Research is required that examines the
potential of genetically based features to evoke particular environments, using bi-directional models. Longitudinal research is also
needed to allow a consideration of developmental pathways
through which differences among children (both genetically and
environmentally influenced) influence the parents' behavior, and
vice versa, in patterns that unfold over time.
Adverse prenatal experiences mechanisms. How strong is the
support for the role of innate dysfunctional neuroregulatory mechanisms in the transmission of risk for depression from depressed
mothers to their children? Overall, the support for this mechanism
is mixed. There is evidence that depressed women have higher
rates of abnormal pregnancies, especially with regard to the hypersecretion of CRF. However, no studies were found that exam-
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ined the placenta to determine the amount of CRF hypersecretion
to which the fetus had been exposed. Nevertheless, it is also
important to note that the results of a number of studies of infants
born to women who had been depressed during pregnancy indicate
that the babies are exhibiting abnormal functioning at birth. These
studies are important because it is likely that they assessed the
infants' functioning before any adverse consequences of exposure
to the depressed mother had appeared, thus implicating more
strongly the role of abnormal fetal environments.
Moreover, knowledge of the psychobiology of depression justifies concern for infants who, as fetuses, might have been exposed
to CRF hypersecretion. We would expect that the consequences of
such exposure would be manifested in abnormal stress reactivity,
negative behavioral and affective functioning, and abnormal EEG
patterns in the infant. Each of these aspects of functioning is
known to be disrupted in adult depression (e.g., Davidson & Fox,
1988; Gotlib, Ranganath, et al., 1998) and could conceivably
represent markers of risk for depression in the infants (Field, Fox,
et al., 1995). Therefore, further studies are needed examining the
fetal environment, examining how it is associated with neonatal
functioning, and assessing more explicitly and precisely how fetal
environment and neonatal functioning might contribute to risk for
the development of depression. It is also not yet known whether
treatment for depression during pregnancy is associated with a
return to the levels of biochemical functioning of nondepressed
women, with the consequence that the neonate may be unaffected
by what was previously a potentially hazardous intrauterine
environment.
Adverse parenting mechanisms. There is consistent empirical
support to indicate that depressed mothers expose their children to
more negative cognitions, affect, and behaviors than do nondepressed mothers and that, in a number of ways, they are inadequate
partners to meet their children's stage-salient needs. There is also
consistent evidence to indicate that the children of depressed
mothers themselves exhibit maladaptive cognitions, affect, and
behavior. We have little understanding, however, of how the
children of depressed mothers acquire these traits or tendencies, or
of the extent to which these traits and behaviors might mediate
their risk for depression.
Stronger support for this mechanism could be provided by
examining the ways in which exposure to, and interaction with, a
depressed mother might contribute to the child's development of
negative cognitions, affect, and behavior. Alternative interpretations for the child's negative functioning, and especially genetic
explanations, need to be ruled out or considered in an integrative
model. For example, more information is needed concerning the
relative frequency with which depressed mothers and other family
members model and reinforce healthy and unhealthy cognitions,
affect, and behaviors. The nature of the association between parents' negative cognitions, affect, and behavior and child outcomes
would also be tested more directly with studies that are based more
strongly on process-oriented models (Bronfenbrenner, 1986). In
such studies, investigators would examine the extent to which, or
level at which, a mother engages in the putative risk behavior (e.g.,
self-critical statements), and not merely whether the mother is
depressed, with respect to her behavior's association with the
children's demonstration of similar behaviors. The studies examining children's matching of their depressed mothers' affect and
behaviors are important steps in the proposed direction.
Empirical support for this mechanism would also be strengthened by studies examining the prospective associations between
the children's depressotypic cognitions, mood, or behavior and
their subsequent development of depression. The findings reviewed earlier—that depressed mothers display more negative
cognitions, affect, and behavior than do nondepressed mothers and
that their children display more negative cognitions, affect, and
behavior than do children of nondepressed mothers—are necessary
but not sufficient findings to support the hypothesized mechanism.
Following Baron and Kenny (1986), the hypothesized mediating
roles of these constructs could be tested more explicitly in two
phases. The first phase would involve tests of the following hypotheses, some of which have already been subjected to empirical
examination:
Hypothesis Al: Elevated levels of maternal depression are associated
with mothers' greater display of negative cognitions, affect, and
behavior. Empirical support for this component of the mechanism is
strong.
Hypothesis A2: Higher levels of negative cognitions, affect, and
behavior in the mother are associated prospectively with higher levels
of depression in the children. Support for this component of the
parenting mechanism is currently weak. Although several studies have
found that depression in mothers is associated prospectively with
depression in their children, no study was found to have demonstrated
that the depressed mothers' negative cognitions, affect, or behavior
per se predict subsequent depression in their children.
Hypothesis A3: Controlling for Al and A2, the strength of the association between maternal depression and children's depression is
significantly decreased.
Similarly, the following hypotheses would be tested in the
second phase:
Hypothesis Bl: Elevated maternal displays of negative cognitions,
affect, and behavior are associated with more negative cognitions,
affect, and behavior in their children. Support for this component of
the mechanism is strong.
Hypothesis B2: More negative cognitions, affect, and behavior in the
child are associated prospectively with higher levels of depression in
the child. Support for this component is weak. Only one study was
found to have tested this component (Hammen et al., 1988), and it
provided only limited support for this component. Moreover, investigators examining this hypothesis will have to work from a diathesisstress perspective, predicting children's subsequent levels of depression from an interaction of their negative functioning and a stressful
life event (cf. Monroe & Simons, 1991).
Hypothesis B3: Controlling for Bl and B2, the association between
maternal depression and children's depression is significantly decreased. Research meeting these design criteria would have the potential of providing stronger support for the mechanism of negative
cognitions, affect, and behavior in children (regardless of how they
are acquired) in the transmission of risk for depression from depressed
mothers to their children.
Finally, conducting more studies of older children, and particularly adolescents, would have the potential of providing stronger
support for this mechanism. It is critical that we begin to examine
precisely how mothers' depression may negatively affect the nurturance and control, authoritative discipline, and parental monitor-
RISK FOR PSYCHOPATHOLOGY
ing that have been linked to the social and intellectual competence
and mental health of school-aged children (Baumrind, 1971; Maccoby & Martin, 1983; Patterson, 1982). It will also be important to
examine outcomes that might be particularly vulnerable for this
developmental stage. This approach of examining stage-salient
issues has yielded promising results in studies of infants and young
children of depressed mothers, and the approach's extension to
older children is clearly an important direction for future research.
Stressful context mechanism. The empirical support for this
mechanism that proposes that the adverse consequences to children of depressed mothers are a function of exposure to stressful
environments comes primarily from findings that children with
depressed mothers face multiple stressors (Hammen et al., 1987).
It is clear from the results of studies in other literatures, not
specific to depressed mothers, that such stressors (e.g., marital
discord, stressful events, financial strains) have negative consequences for children. What is not yet known, however, is the extent
to which these stressors represent a mechanism through which
children of depressed mothers develop adverse outcomes. Arguably, therefore, this mechanism represents the weakest and least
specific link in the model with respect to empirical validation.
Indeed, none of the studies that examined stress in the families
of children with a depressed mother directly tested a mediational
model. In some studies stress was found to function as a moderator
variable, increasing the strength of the association between maternal depression and negative child outcomes. The single exception
to this general pattern was reported by Hammen et al. (1987),
whose data supported an additive rather than a moderator model,
with maternal depression and stress both having cumulative negative effects on child functioning.
Empirical support: Robustness of components. In sum, none
of the specific mechanisms that we have delineated in this article
has received unequivocal support by the empirical literature. Although many of the strongest findings for the model represent
empirical support for specific components of the proposed mechanisms, little research has examined the mediational role specified
by the mechanism. For example, an important component of each
mechanism is the link between maternal depression and the mechanism. Across all mechanisms, this component was found to have
strong support. Thus, we found maternal depression consistently to
be associated with heritability of depression; with adverse prenatal
experiences; with multiple aspects of adverse parenting in the
domains of cognition, affect, and behavior; and with stressful life
experiences.
The association between the mechanisms and the development
of depression or other psychopathology in the children has received considerably less empirical attention. The genetics mechanism is one of the few for which relevant studies were available,
that is, studies of the genetic contribution to childhood depression.
Interestingly, the results of some of these studies indicate that there
may not be a strong heritability component for childhood depression, at least in certain subsamples. The mechanism implicating
adverse prenatal experience in the transmission of risk from depressed mother to child has received strong empirical support from
the studies on nonhuman primates and rodents but has not yet been
investigated in humans. The associations between the development
of depression in the children and exposure to both adverse parenting and stressful environments have not yet received adequate
empirical attention.
477
Finally, all of the proposed mechanisms have received at least
some empirical support with respect to their association with the
vulnerabilities described in the model. The genetics mechanism is
supported by the findings of strong heritability for many of the
environmental and personal characteristics that increase vulnerability to depression. The adverse parenting mechanism is supported by findings of a strong association between the adverse
parenting of depressed mothers and skills deficits or maladaptive
cognitive, affective, and behavioral styles or tendencies in the
children. The adverse prenatal experiences and stressful context
mechanisms have received less direct empirical support. Thus, a
number of studies have reported a strong association between
abnormal pregnancies in women experiencing stress, rather than
depression per se, and abnormal functioning of the neonate. Similarly, support for the stressful context mechanism comes from
studies that examined the consequences for children of exposure to
various stressors but that were not specific to maternal depression.
More broadly, research relevant to the key component to establish mediation, the functional roles of the mechanisms, has not yet
been conducted. We rarely found studies that directly tested mediation as a causal mechanism, either statistically using correlational data (Baron & Kenny, 1986; Holmbeck, 1997) or as a
function of experimental manipulations, such as prevention experiments. These studies are clearly important, not only because they
have the potential to provide support for the mechanisms proposed
in this article but also because they may fail to confirm hypotheses,
thus allowing for determination of the falsifiability of a putative
mechanism.
It is also important to examine the extent to which the mechanisms are associated with adverse outcomes in the children. In this
context, the concept of "dosage" might be helpful. For example,
with respect to genetics, the number of first- or second-degree
relatives with depression is likely to be an important variable.
Similarly, the extent of exposure to self-critical statements or
mother's sad affect, and the degree of adversity in the environment, may be important with respect to the parenting and stress
mechanisms. Quantitative examinations of th'ese aspects of the
mechanisms proposed in this article could address such questions
as, "How much exposure to (self-) critical statements is needed to
result in specific negative effects on the child's cognitions and
affect?"
Finally, when investigators examine the mechanisms proposed
in this article, it will be important that they examine the functioning of clinically depressed women and their children, rather than
rely on the more commonly studied samples of women who obtain
high scores on self-report depression symptom or mood scales. We
have noted the critical importance of this distinction throughout
this article, and it is further underscored by Harrington et al.'s
(1996) recent review of epidemiologic and adult outcome differences between depression as a mood feature and depression as a
diagnostic category. For example, Harrington et al. reported that
84% of children who had a full depressive syndrome in childhood
had the same syndrome in adult life. In contrast, although there
was also strong continuity at the symptom level, at both age
periods depressive symptoms were associated with a wide range of
psychopathology other than depression. That is, depressed mood
appeared to be a nonspecific indicator of psychopathology. In
another set of studies, Harrington et al. reported that the age and
gender trends that were found to characterize the diagnostic cate-
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GOODMAN AND GOTLIB
gory of depressive disorder did not apply to findings derived from
questionnaire measures of depressed mood. Summarizing these
findings, Harrington et al. concluded that a diagnosis of depression
is different in a number of important respects from depression as
measured by questionnaires.
Level of Theory
In a sense, each of the proposed mechanisms offers a minitheory of how depressed mothers affect their children. Similarly,
each of the proposed moderators offers a mini-theory of the
circumstances under which children might be more or less affected
by maternal depression. Indeed, most of the literature examining
the effects of maternal depression on child functioning has taken
the approach of studying one particular aspect of this association
and, sometimes, generating small-scale theories focused on the
particular processes under study.
In contrast to this approach, we argue strongly for the advantages of the additional explanatory power that comes from a model
that provides a larger, more integrative picture of the transmission
of risk from depressed mothers to their children. The more molecular approach, we believe, leaves us in a situation like the
proverbial blind men and the elephant, in which each man, having
touched a different part of the creature (e.g., a leg versus the trunk
versus the tail), erroneously generalized from that experience to an
innaccurate conceptualization of the elephant's true nature. The
approach leads to difficulties associated with reductionism and
dualism (e.g., biological versus psychosocial functioning). In contrast to these more restrictive perspectives, the model proposed,
described, and evaluated in this article provides guidelines for
exploring how the mechanisms interrelate and thus yields unique
predictions. In this context, many theorists in psychology have
been moving toward merging previously separate, narrow foci in
attempts to provide stronger explanations of behavior. In particular, theorists are increasingly combining diverse biological and
environmental processes and emphasizing their dynamic interplay
(Zahn-Waxier, 1996). Transactional, multifaceted models have
been the hallmark of much of recent research on developmental
psychopathology. Unfortunately, measurement and research design become more complicated as researchers attempt to test
those complex models. The model proposed in this article poses
similar challenges; suggestions for relevant and illuminating research are unlikely to involve studies that are quickly and easily
implemented.
That said, the integrative model presented in this article does
raise important questions concerning the possible interrelations
among the mechanisms. For example, does each aspect or component of the nonoptimal parenting mechanism operate as "stress"
in a stress-diathesis model? If so, what are the diatheses? Possibilities that are suggested by the model include psychobiological
vulnerabilities, such as lowered vagal tone, abnormal stress response, reduced left frontal activity, or genetically influenced
tendencies, such as behavioral inhibition and negative affectivity.
From the broader perspective of the integrative model, it is
apparent that the genetics studies that we reviewed are limited by
their exclusive focus on attempting to estimate how much heritability contributes to individual differences. It is clear that the field
of behavior genetics studies has the potential to make much greater
contributions than it has to date to the understanding of the
functioning of children with depressed mothers (Rutter, Silberg, &
Simonoff, 1993). For example, it is essential that any integrative
model of the transmission of risk to children of depressed mothers
include the genetic contribution to the experience of stressful life
events and other aspects of the family environment that have been
firmly established as significant correlates of parental depression.
Moreover, as suggested in our model, studies are needed that
explore gene-environment covariation, including the possibilities
that siblings may be treated differently by the same depressed
parent, that children of depressed parents may both seek and evoke
certain qualities in their environments, and that at-risk children
may "experience" their environments differently than do children
of well parents. Although we found some support for the first of
these possibilities, the latter two possibilities have yet to be explored systematically.
In gaining a more comprehensive understanding of the functioning of children of depressed mothers, it will also be important to
identify exactly what it is that these children inherit. In this
context, one promising research direction would be an integration
of the conceptualization of biological trait markers with recent
formulations concerning inborn neurobiological mechanisms. In
an integrated model, there are two alternative pathways for the
influence of biological trait markers that represent a vulnerability
to depression: (a) The vulnerability manifests itself in behavior
only in the context of maladaptive environments (e.g., inadequate
parenting of infants; stress or hormone fluctuations during adolescence), or (b) the vulnerability is expressed in behavioral traits or
tendencies that are evident at birth and that then become part of
evocative, gene-environment correlations (e.g., the children engage the environment less actively or less positively; children
selectively attend to, or are more sensitive to, negative aspects of
their environment).
The first pathway, that vulnerability manifests itself only in
maladaptive environmental contexts, is compatible with promising
gene-environment interaction models, such as the stress-diathesis
model (e.g., Monroe & Simons, 1991). Walker et al. (1996)
explicated a relevant model that focuses on the moderating role of
stress exposure and reactivity (i.e., biological stress responses) in
the expression of the organic diathesis for schizophrenia. The
stress-diathesis model, approached with a consideration of developmentally sensitive time periods, suggests, for example, that
maladaptive early parenting could result in the behavioral manifestation of a biological vulnerability in infants that would otherwise have remained unexpressed. Similarly, offspring who, by
adolescence, have not yet manifested signs of illness, could experience a "turning on" of the biological vulnerability, perhaps
through hormonal influences or through the accumulation of stressors. Indeed, this model may help to explain the potential role of
genetics in contributing to the increased prevalence of depression
that emerges for girls at puberty (cf. Hayward, Gotlib, Schraedley,
& Litt, 1998).
Even less is known about how the second pathway, geneenvironment correlations, might function in children of depressed
mothers. If biological vulnerabilities can be measured reliably, it
will be possible to test whether children with these vulnerabilities
are more sensitive to the effects of environmental stressors than are
their nonvulnerable counterparts. In general, we know little about
how the relative importance of genetic and environmental risk
factors might change over the course of development. From a
RISK FOR PSYCHOPATHOLOGY
genetic perspective, research designs that take advantage of psychiatric or twin registries, such as those used by Crowe (1975),
Cloninger and his colleagues (e.g., Cloninger, Sigvardsson, Bohman, & von Knotting, 1983), and Kendler and Kessler and their
colleagues (e.g., Kendler et al., 1993), would be useful in examining whether genetically vulnerable children are more susceptible
than others to adverse environmental stressors, and those research
designs would enable researchers to test for variations in such
associations in children at different periods of development.
To date, no studies have tested the more specific hypothesis of
concordance for depression in offspring of affected (i.e., depressed) and unaffected monozygotic twins. Such research would
help to delineate the developmental course of offspring who share
the genetic risk of their cousins with a depressed parent but who
may not experience the family environment correlates of parental
depression. Indeed, the extent to which the unaffected twin-parent
provides similar or different family environment experiences for
his or her offspring is itself an unaddressed empirical question.
Other interesting questions arise regarding the processes that
might unfold as a function of being born with greater or lesser
genetic vulnerability to depression and of then being raised by a
mother who experiences depression at some point(s) in the child's
life. Weissman (1988), for example, suggested that whereas offspring of depressed mothers may follow a genetic pathway to
depression, children of nondepressed mothers who become depressed may follow an environmental (family risk factors) pathway. To date, however, this thesis has not been examined
empirically.
Another hypothesis concerning multiple mechanisms of transmission of risk suggested by the integrative model presented in this
article is that cognitive-interpersonal influences, or more specifically, parenting behaviors, may be stronger determinants of children's functioning for those children who are not at the extremes
on either genetically or prenatally caused behavioral traits or
regulatory styles. At the extremes, it is likely that parents are less
influential in determining their children's outcomes (Calkins, Fox,
& Marshall, 1996; Deiter-Deckard & Dodge, 1997). Conversely,
the extremes of parenting or the caregiving situation (e.g., abuse)
will, in general, override the importance of children's characteristics, conferring vulnerability even to children without genetic or
prenatal risks (Calkins, 1994).
It will also be important to determine whether supportive parenting might modify the risk for the development of depression in
high-risk children who are identified early as having any of
the hypothesized neurobiological vulnerabilities. For example,
Thompson (1994) and Calkins (1994) suggested that risk for
psychopathology may be reduced through a number of means,
such as direct interventions for parents aimed at reducing negative
emotions, modeling or selective reinforcement of the children's
expressions of positive emotions, verbal instructions concerning
positive emotion and emotion regulation strategies, and limiting
the demands on the child early on in order to reduce the probability
of negative emotional arousal. Importantly, depressed mothers
have already been found to be deficient in several of these parenting supports. For example, compared with their nondepressed
counterparts, depressed mothers make more negative attributions
about their children during mother-child interactions (RadkeYarrow et al., 1990) and use more guilt induction and anxiety
479
induction as discipline practices, thereby likely increasing their
children's feelings of responsibility, guilt, and helplessness.
Studies are also required that explore how the four mechanisms
proposed in this article might interact in conferring risk to children
of depressed mothers. For example, the neuroregulatory dysfunctions that have been found at birth in the infants of depressed
mothers have important implications in light of predictions generated by the parenting mechanism, providing more opportunities
for exploring the integration of these two mechanisms. Children
who look "depressed" (i.e., are lethargic, affectively flat, and
irritable) likely require more arousing stimuli to elicit responses,
and they are less likely to actively engage their environments, to
focus their attention on learning opportunities, to cope with stress,
and to evoke positive responses from their parents and peers.
Moreover, given the characteristics of negative cognitive biases,
such children are likely to selectively attend to negative aspects of
the environment, to experience elevated levels of stress and sadness, and to withdraw rather than use active social or cognitive
strategies for coping (cf. Gotlib & MacLeod, 1997), thereby also
implicating cognitive mechanisms in the transmission of risk.
Other examples of questions that cut across a number of these
mechanisms are those being explored by Dawson and her colleagues concerning the influence of early adverse parenting on
psychobiological vulnerabilities (e.g., Dawson et al., 1997; Dawson et al., 1994), and by Forges, Fox, and their colleagues (e.g.,
Fox, 1994; Forges, 1992; Forges et al., 1994) examining how
infants' vagal tone might be related both to their emotion regulation abilities (e.g., their abilities to self-soothe and to explore novel
stimuli) and to the likelihood that they will have behavior problems 2 years later. With respect to the latter question, the presence
or relative strength of one or another mechanism may predict
whether the child develops depression or, for example, conduct
disorder. We discuss this issue of differential outcome in greater
detail below.
The model also highlights the need for studies that examine the
transactional aspects of the proposed mechanisms. More specifically, investigations are required that examine how the mediators
are likely to interact and feed back to one another over the course
of development. For example, although dysfunctional cognitions
have been linked to behaviors that increase risk for depression,
these associations have not been examined systematically in the
offspring of depressed parents. Studies are also required that assess
how the vulnerabilities of the offspring feed back to the parenting
system, perhaps increasing the parents' stress, decreasing their
sense of parenting efficacy, and adversely affecting the quality of
parent-child interactions.
Another example of work that might benefit from the integrative
model presented in this article is the research on neuroregulatory
difficulties in infants with depressed mothers. Field and Dawson
and their colleagues have found that infants of depressed mothers
have lower vagal tone and reduced left frontal activity, important
indexes of vulnerability to depression. An "environmental" interpretation of these two findings would be that they both reflect the
negative effects of the stress of interacting with a nonresponsive,
less synchronous, or irritable depressed mother. It is important to
note, however, that these findings are also consistent with the
operation of other mechanisms, such as genetically based or in
utero environmental-based physiological differences in neural regulation. With either of the latter mechanisms, the deficit or dia-
480
GOODMAN AND GOTLIB
thesis either could become manifest only under the conditions of
experience with a depressed mother or, alternatively, could be
exacerbated by those experiences. Exploration of such transactions
among mechanisms is likely to be much more profitable than
further efforts to determine whether adverse parenting or preexisting biological vulnerability provides a stronger explanation for
the neuroregulatory difficulties observed among children with
depressed mothers.
Other similar questions are suggested by the moderators in the
model. For example, as we reviewed above, several investigators
have found that the specific stressor of marital discord is related to
children's difficulties more strongly than is maternal depression
(cf. Lee & Gotlib, 1991b). Nevertheless, more research is required
examining how marital conflict and parental depression may interact in ways that are related to the emergence of psychopathology in the children. In this context, Gottman's (e.g., Gottman et al.,
1996) recent work on meta-emotion represents a potentially useful
direction.
Finally, the integrative model presented in this article also
provides a conceptual context within which to consider bidirectional influences. More specifically, the moderators described
in this model could be tested for bi-directional effects. For example, research is clearly required examining children's influences on
their mothers' depression. There have been some suggestions of
such bi-directionality in mothers of infants who are difficult in
temperament, whereby the infant might contribute to or exacerbate
the mother's depression (Cutrona & Troutman, 1986). The model
raises other questions about how children with the particular
vulnerabilities might affect their parents and others, who then
influence the child in a dynamic interplay. Although some studies
have examined such dynamics in a molecular way, such as the
mother-infant studies or Hops's (1996) study of behavioral contingencies in family interactions, none has explored the longitudinal associations.
Specificity of the Model to Depression
There are two important aspects to the issue of specificity: the
specificity of maternal depression as a risk factor for child depression and the specificity of child depression as an outcome of the
impact of maternal depression. And even within this issue of the
specificity of maternal depression as a risk factor, there are questions concerning the impact of depression versus other forms of
psychopathology and the impact of depression versus confounded
correlates of depression. There is little question that forms of
psychopathology other than depression are associated with adverse
outcomes in the offspring. Indeed, the field of high-risk research
arguably began with the study of the effects of schizophrenia in the
parent on children (e.g., Mednick & Schulsinger, 1968) and has
since included investigations examining the impact of parental
depression, anxiety, and alcoholism (cf. Gotlib & Avison, 1993).
Much less research has examined the extent to which the mother's
depression per se, rather than specific correlates of maternal depression, affects the children. Among the common correlates of
depression that require consideration are poverty, co-occurring (or
comorbid) disorders such as alcohol or drug abuse, general negative affectivity, marital conflict, and other stressors.
One correlate of maternal depression that has been studied more
broadly than others is marital conflict. Thus, for example, as we
noted earlier, Grych and Fincham (1990) and Katz and Gottman
(1993) presented data indicating that marital conflict in the parents
results in increased hostility and decreased availability of the
parents to their children, which in turn increases the risk to the
children for both internalizing and externalizing behavior problems. However, this formulation has not been examined explicitly
among children of depressed parents. As we discuss in more detail
below, if these findings are replicated among families with depressed mothers they would also have implications for the issue of
the breadth or specificity of the effects on the children.
The relative impact of another important correlate of depression,
poverty, has not been examined directly. Indeed, because poverty
and depression have been confounded in previous studies, it is
virtually impossible to examine differential effects of these two
variables. In addition, in many of the studies in which depression
is confounded with poverty, both these variables were also confounded with ethnic minority status. For example, both Field and
Lyons-Ruth, who have made major contributions to the study of
the impact of maternal depression on offspring, included a large
proportion of ethnic minority women in their samples of lowerclass depressed women. It is very difficult in such studies to test
the relative contribution of maternal depression, poverty or stressors associated with poverty, and belonging to an ethnic minority
to adverse consequences for the children.
Clearly, therefore, future studies should include an explicit
assessment of critical correlates of depression, ideally sampling
across these correlates to permit testing of their relative contribution to the child outcome, both alone and in interaction with
maternal depression. A consideration of these correlates is also
important in the choice of control or comparison groups. Without
assessing correlates of maternal depression, it is likely that group
comparisons are overestimating the impact of the mother's depression. An example that nicely illustrates this point is Hammen's
(1991) finding that stress should be treated as a separate and
important predictor of outcome in children with depressed mothers. Ideally, future studies will provide a more complete understanding of the extent to which maternal depression exerts a unique
impact on the children.
The second aspect of this issue, the question of specificity of
outcome to the children, has also received little attention. It is
important that a comprehensive theory ultimately be able to account for alternative outcomes in children of depressed mothers.
Although a higher proportion of children of depressed mothers
develop depression than is the case for children of nondepressed
mothers, researchers have also documented higher rates of externalizing disorders among children of depressed mothers (cf. Hammen, 1991; Lee & Gotlib, 1989); indeed, researchers have described some children of depressed parents, as young as infants, as
angry rather than withdrawn (e.g., Cohn & Campbell, 1992; Field
et al., 1990). The reasons for this anger are not yet well understood, but it seems reasonable to hypothesize that it might be a
function of the frustration that infants and children likely experience in not having their needs met by their depressed mothers.
Some theorists have speculated about specific conditions under
which these outcomes might vary and have considered such factors
as heredity, particularly with respect to the mother's comorbidity
of depression with other psychiatric disorders, the overlay of
RISK FOR PSYCHOPATHOLOGY
marital problems, the age of the child when first exposed to the
mother's depression, and the other moderator variables in our
proposed model. For example, the varying outcomes in the children may be explained by heritability that is not specific to
depression. Thus, children with depression and disruptive behavior
disorders or substance abuse disorders may have relatives who
themselves have had depression that is comorbid with alcoholism,
substance abuse, or antisocial personality disorder (e.g., Kovacs et
al., 1997; Williamson et al., 1995).
Diverse outcomes in the children could also reflect a different
relative contribution of genetic and environmental influences. For
example, Fendrich et al. (1990) found that among 6- to 23-yearolds of depressed parents, parent-child discord and low family
cohesion were significant predictors of conduct disorder but not of
any other psychiatric disorder. Findings such as these can be
interpreted as suggesting that externalizing disorders in the offspring of depressed parents represent the expression of the genetic
risk when it is combined with the relatively high rates of environment risks that exist in families with depressed mothers. It is
important that Fendrich et al.'s finding be replicated in a sample
with a narrower age range and with risk factors that follow from a
conceptual model, such as that presented here. It is also important
to rule out the bi-directional effect of the child on the parent or on
the risk factors, for example, that more of the variance in parentchild discord is due to the child's conduct problems than to the
depressed parent per se.
Another clue to specificity of outcome of children of depressed
mothers comes from the finding of a number of studies that
depression and externalizing disorders might share common biological underpinnings. For example, McBurnett et al. (1991) found
that the cortisol levels of 8- to 16-year-old boys with pure anxiety
disorders were no higher than were those of control children. In
contrast, boys with both anxiety and conduct disorders had elevated cortisol levels relative to the other clinically diagnosed
participants. Thus, HPA reactivity in childhood may be related to
negative affect more broadly, rather than only to those negative
affects that are associated more specifically with unhappiness and
anxiety.
It is also possible that these various outcomes are a function of
the frequent co-occurrence of depression with marital discord and
its associated increase in interparental and parent-child hostility
and decreased parental availability (cf. Lee & Gotlib, 1991b). We
discussed above the importance of examining marital discord in
the context of assessing correlates of maternal depression, but it is
likely that marital discord also affects the specificity of child
outcome. Earlier in this article we described studies demonstrating
that children's problems are related more strongly to parental
marital discord than to maternal depression (e.g., Caplan, 1989;
Cox et al., 1987; Emery et al., 1982); we also described studies
indicating that marital discord increases the risk for both internalizing and externalizing behavior problems in children (e.g., Grych
& Fincham, 1990; Katz & Gottman, 1993). Studies of depressed
mothers who vary in the presence of discord in their marriages
would illuminate the relative contribution of depression and marital discord to both conduct disorder and depression in their children (Downey & Coyne, 1990).
Finally, our model provides reason to consider that the other
moderator variables, in addition to child's age or timing of the
exposure, may also help to explain different outcomes for children
481
of depressed mothers. For example, antisocial personality disorder
in the fathers of children with depressed mothers could increase
the likelihood of disruptive behavior disorders in the children,
either alone or comorbid with depression (e.g., Lahey et al., 1988).
Other characteristics of the children such as their temperament,
gender, and intellectual and social-cognitive skills could also influence their outcome. For example, Cummings and Da vies (1994)
implicated gender role modeling as an explanation for what appears to be an increased vulnerability to depression among daughters of depressed mothers and an increased vulnerability to conduct
problems among their sons.
In general, from a methodological perspective, if child depression is the only outcome that is studied and if maternal depression
status is the only predictor variable, the opportunity to determine
whether adverse consequences to the children are specific to
maternal depression is missed. Moreover, the onset of depression
(or of any other disorder) is typically marked by specific antecedents, such as the vulnerabilities that are proposed in this model. In
this context, research would also benefit from studies that examine
vulnerabilities as intermediate outcomes, testing whether they mediate the association between the mechanisms and psychiatric or
emotional outcomes. It will be particularly important to test
whether specific mechanisms, or particular combinations of the
mechanisms, are associated with specific vulnerabilities and, if so,
whether those vulnerabilities are associated with specific outcomes
for the children. Finally, studies that predict which children will
remain well despite the presence of the putative mechanisms (and
vulnerabilities) will be critical in understanding the processes
involved in translating risk into overt psychopathology.
Sensitive Periods and Recovery From Adversity
The final issue we raise and discuss here concerns the concept
of critical ages, or sensitive periods, and the possibilities for
children to "recover" from the adversities associated with maternal
depression. This issue arises from our concern that our proposed
model of the transmission of risk (a) be sensitive to development
and (b) be able to explain how risk might differ for children at
different ages and explain how the transactional relations between
risk and the emergence of psychopathology unfold over time.
The issue of the timing of the child's exposure to parental
depression clearly requires further investigation. Studies such as
that conducted by Alpern and Lyons-Ruth (1993) need to be
replicated and extended to gain a better understanding of the
importance of maternal depression that occurs early in a child's
life. For example, it might be possible to examine the impact of
this type of maternal depression by studying a high-stress sample
of women who are at elevated risk for depression, such as women
living in poverty. A significant proportion of such a sample of
women would be expected to become depressed within, for example, 5 years. Thus, comparisons could be made among children
whose mothers were never depressed in their first 5 years of life,
children whose mothers were depressed early in their lives but had
recovered at the time of assessment, and, most importantly, children whose mothers were not depressed in their first year of life
but who became depressed thereafter. The roles of adverse parenting and other stressors would also be illuminated through
studies of children who are similar in familial loading for depression but who vary with respect to the age at which they were first
482
GOODMAN AND GOTLIB
exposed to maternal depression. For example, by the age of 8 or 9,
children have formulated fairly stable self-perceptions and attributional beliefs (Digdon & Gotlib, 1985; Harter, 1983; Seligman &
Peterson, 1986) and, therefore, may be less vulnerable at this age
to a first exposure to a depressed parent's depressotypic cognitions
and criticisms.
The older child or adolescent also requires special consideration.
One important issue involves an interesting variation on the confound between environmental and genetic contributions to risk.
More specifically, if a mother experiences a first onset of depression when her child is an adolescent, it is likely that the mother will
be older than are mothers who become depressed when their
children are infants or toddlers. In this context, it is important to
note that age of onset for depression is significantly associated
with familial loading (Weissman et al., 1984). Thus, the older the
child when first exposed to parental depression, the less the environmental exposure and the less the genetic (and in utero environmental) risk to that child. It is clear that we require studies of
children who are older when they are first exposed to their mother's depression and who differ on familial loading for depression.
Given that the median age of onset for depression in women is 23
years (Burke, Burke, Regier, & Rae, 1990), that is, in the midst of
childbearing years, it should be possible to identify samples of
children who vary with respect to the age at which they were first
exposed to maternal depression.
The age of the child is relevant not only in terms of the timing
of the parent's depression, but also more broadly, with respect to
the developmental tasks faced by children at various ages. As we
discussed earlier,, infants are particularly vulnerable to the effects
of maternal depression at least in part because their neuroregulatory mechanisms are still developing. It is important to be cognizant of the fact that although these mechanisms may be most
strongly influenced during the period in which there is still considerable plasticity, once affected they will continue to have an
impact on further development. That is, once they are affected, the
operation of inadequately functioning neuroregulatory mechanisms has critical implications for subsequent functioning. We are
just beginning to understand how these early alterations may result
in permanently reduced adrenocortical responses to subsequent
stressors (cf. Heim, Owens, Plotsky, & Nemeroff, 1997). Such
children would be expected to exhibit a state of sensitization to
stress; ultimately, this vulnerability would be predicted to lead to
an increased risk for development of depression. In a similar
manner, children who acquire dysfunctional cognitions as a consequence of early exposure to maternal depression may have
difficulty altering those negative beliefs even after the mother
recovers from depression. Finally, children who withdraw from
their peer group and later attempt to re-enter the group may have
missed critical opportunities to learn social skills and may not be
readily "re-accepted" by their peers.
Adolescent offspring of depressed parents also offer important
opportunities for testing hypotheses generated by our proposed
integrative model. Rates of depression increase at adolescence for
offspring of depressed parents, as they do in the general population. It is not known, however, whether this increase reflects a
"switching on" of the genetic vulnerability to depression or an
interaction of genetic vulnerability either with pubertal onset or
with the increased stressors of that time period. Thapar and
McGuffin's (1996) finding of greater heritability of adolescent
than of childhood depression needs to be considered within this
context. Tests of the interactions of parental depression with offspring age and pubertal status would elucidate whether children
with depressed parents are at increased risk for adolescent-onset
depression. In this context, further exploration of the increased risk
of depression for girls would also be important.
Another avenue that must be pursued with regard to the timing
of the mother's depression concerns the differential effects of
various "clusters" or subtypes of maternal depressive symptoms on
children of different ages. That is, it would be important to know
whether the predominant symptoms of a depressed mother,
whether they be depressed mood, somatic concerns, or negative
cognitions, have a more negative influence on the adjustment of
younger children than on the adjustment of older children. Mediational models could be tested as well, such as whether a depressed
mother's inadequate monitoring and discipline of her child is
mediated by the mothers' negative view of herself as a parent (e.g.,
Jaenicke et al., 1987; Kochanska, Radke-Yarrow, et al., 1987; Teti,
Gelfand, & Pompa, 1990; Webster-Stratton & Hammond, 1988).
In general, increased developmental competencies may work both
to children's advantage (increased ability to understand a stressful
situation) and to their disadvantage (increased vulnerability to
negative cognitions with age). It remains for future research to
examine this issue more explicitly.
Summary
In this article, we proposed a developmentally sensitive, integrative model for understanding the mechanisms and moderators
that might underlie the transmission of risk for psychopathology
and abnormal development in children of depressed mothers. In
presenting this model, we examined and evaluated empirical findings with respect to the extent to which they support each of the
proposed mechanisms and moderators. We concluded by raising
and discussing four issues that confront the field and by suggesting
promising directions for future research in this area.
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Received February 18, 1997
Revision received June 12, 1998
Accepted September 6, 1998 •
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